blm induction Search Results


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Thermo Fisher apr 1 expression blm apr 1 cell
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MedChemExpress blm induced senescence research
PRDM16 was decreased in aged organs and SnCs. a) qPCR analysis of PRDM family members in the kidneys, lungs, heart and stomach of young (2 months old) and aged (24 months old) mice (n = 3). b) qPCR analysis of Prdm16 in multiple organs of 2 months mice (n = 6). c) Analysis of one published transcriptomic dataset showed that PRDM16 decreased with age in human normal renal cortex (n = 71). d–f) Tests for linear trend were conducted between age and PRDM16 mRNA level in the heart (d) (n = 384), brain hippocampus (e) (n = 187) and lung (f) (n = 345) of humans based on transcriptomes from ADEIP. g) Correlational analysis of PRDM16 mRNA level (log 10 (2 −(ΔΔCt) )) and age in human normal lung samples (n = 13). h) Correlational analysis of the mRNA levels (log 10 (2 −(ΔΔCt) )) of PRDM16 and CDKN1A in human normal lung samples (n = 13). i) qPCR analysis of Prdm16 in the kidneys, lungs, brain hippocampus and heart of 2 months old (2 M) and 24 months old (24 M) mice (n = 6). j) Representative immunohistochemical (IHC) staining images of PRDM16 in the kidney of 2 months and 24 months mice. Scale bar: 50 µm. k) Diagram detailing X‐ray radiation, <t>BLM</t> and DOX induced cellular <t>senescence.</t> l) qPCR analysis of Prdm16 in senescent HK‐2, Beas‐2B and H9C2 cells (n = 3). Data are mean ± SEM. * p < 0.05, ** p < 0.01 and *** p < 0.001. Spearman's correlations (c, g and h), Test for linear trend (d–f), Two‐tailed Student's unpaired t ‐test analysis (i and l).
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Mead Johnson blm blenoxane
PRDM16 was decreased in aged organs and SnCs. a) qPCR analysis of PRDM family members in the kidneys, lungs, heart and stomach of young (2 months old) and aged (24 months old) mice (n = 3). b) qPCR analysis of Prdm16 in multiple organs of 2 months mice (n = 6). c) Analysis of one published transcriptomic dataset showed that PRDM16 decreased with age in human normal renal cortex (n = 71). d–f) Tests for linear trend were conducted between age and PRDM16 mRNA level in the heart (d) (n = 384), brain hippocampus (e) (n = 187) and lung (f) (n = 345) of humans based on transcriptomes from ADEIP. g) Correlational analysis of PRDM16 mRNA level (log 10 (2 −(ΔΔCt) )) and age in human normal lung samples (n = 13). h) Correlational analysis of the mRNA levels (log 10 (2 −(ΔΔCt) )) of PRDM16 and CDKN1A in human normal lung samples (n = 13). i) qPCR analysis of Prdm16 in the kidneys, lungs, brain hippocampus and heart of 2 months old (2 M) and 24 months old (24 M) mice (n = 6). j) Representative immunohistochemical (IHC) staining images of PRDM16 in the kidney of 2 months and 24 months mice. Scale bar: 50 µm. k) Diagram detailing X‐ray radiation, <t>BLM</t> and DOX induced cellular <t>senescence.</t> l) qPCR analysis of Prdm16 in senescent HK‐2, Beas‐2B and H9C2 cells (n = 3). Data are mean ± SEM. * p < 0.05, ** p < 0.01 and *** p < 0.001. Spearman's correlations (c, g and h), Test for linear trend (d–f), Two‐tailed Student's unpaired t ‐test analysis (i and l).
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blm  (ApexBio)
90
ApexBio blm
PRDM16 was decreased in aged organs and SnCs. a) qPCR analysis of PRDM family members in the kidneys, lungs, heart and stomach of young (2 months old) and aged (24 months old) mice (n = 3). b) qPCR analysis of Prdm16 in multiple organs of 2 months mice (n = 6). c) Analysis of one published transcriptomic dataset showed that PRDM16 decreased with age in human normal renal cortex (n = 71). d–f) Tests for linear trend were conducted between age and PRDM16 mRNA level in the heart (d) (n = 384), brain hippocampus (e) (n = 187) and lung (f) (n = 345) of humans based on transcriptomes from ADEIP. g) Correlational analysis of PRDM16 mRNA level (log 10 (2 −(ΔΔCt) )) and age in human normal lung samples (n = 13). h) Correlational analysis of the mRNA levels (log 10 (2 −(ΔΔCt) )) of PRDM16 and CDKN1A in human normal lung samples (n = 13). i) qPCR analysis of Prdm16 in the kidneys, lungs, brain hippocampus and heart of 2 months old (2 M) and 24 months old (24 M) mice (n = 6). j) Representative immunohistochemical (IHC) staining images of PRDM16 in the kidney of 2 months and 24 months mice. Scale bar: 50 µm. k) Diagram detailing X‐ray radiation, <t>BLM</t> and DOX induced cellular <t>senescence.</t> l) qPCR analysis of Prdm16 in senescent HK‐2, Beas‐2B and H9C2 cells (n = 3). Data are mean ± SEM. * p < 0.05, ** p < 0.01 and *** p < 0.001. Spearman's correlations (c, g and h), Test for linear trend (d–f), Two‐tailed Student's unpaired t ‐test analysis (i and l).
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96
Selleck Chemicals immunology 03 bleomycin induced lung injury model bleomycin sulfate
PRDM16 was decreased in aged organs and SnCs. a) qPCR analysis of PRDM family members in the kidneys, lungs, heart and stomach of young (2 months old) and aged (24 months old) mice (n = 3). b) qPCR analysis of Prdm16 in multiple organs of 2 months mice (n = 6). c) Analysis of one published transcriptomic dataset showed that PRDM16 decreased with age in human normal renal cortex (n = 71). d–f) Tests for linear trend were conducted between age and PRDM16 mRNA level in the heart (d) (n = 384), brain hippocampus (e) (n = 187) and lung (f) (n = 345) of humans based on transcriptomes from ADEIP. g) Correlational analysis of PRDM16 mRNA level (log 10 (2 −(ΔΔCt) )) and age in human normal lung samples (n = 13). h) Correlational analysis of the mRNA levels (log 10 (2 −(ΔΔCt) )) of PRDM16 and CDKN1A in human normal lung samples (n = 13). i) qPCR analysis of Prdm16 in the kidneys, lungs, brain hippocampus and heart of 2 months old (2 M) and 24 months old (24 M) mice (n = 6). j) Representative immunohistochemical (IHC) staining images of PRDM16 in the kidney of 2 months and 24 months mice. Scale bar: 50 µm. k) Diagram detailing X‐ray radiation, <t>BLM</t> and DOX induced cellular <t>senescence.</t> l) qPCR analysis of Prdm16 in senescent HK‐2, Beas‐2B and H9C2 cells (n = 3). Data are mean ± SEM. * p < 0.05, ** p < 0.01 and *** p < 0.001. Spearman's correlations (c, g and h), Test for linear trend (d–f), Two‐tailed Student's unpaired t ‐test analysis (i and l).
Immunology 03 Bleomycin Induced Lung Injury Model Bleomycin Sulfate, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Nippon Kayaku bleomycin
The effect of Longidaze on the hematological parameters of C57BL/6 mice modeling <t>bleomycin-induced</t> pulmonary fibrosis on d7. Hematological parameters after pirfenidone administration per os, after intramuscular ( a ) and intranasal ( b ) administration of different doses of Longidaze. Groups of mice: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal. WBCs—white blood cells (10 9 /L blood); GRA 10 9 , LYM 10 9 , MON 10 9 (absolute number), GRA %, LYM %, MON % (relative number)—number of neutrophils, lymphocytes, monocytes; RBCs 10 12 —red blood cells (10 12 /L blood). Statistical analysis of data was performed using the Kruskal–Wallis test, post hoc Wilcoxon test for pairwise comparisons with bleomycin control group (with corresponding route of administration), and Bonferroni correction (ns— p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).
Bleomycin, supplied by Nippon Kayaku, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Nippon Kayaku blm
Decreased CD45 − /ALDH br <t>during</t> <t>pulmonary</t> fibrosis. A Lung hydroxyproline content on day 14 in the PBS ( n = 4) and the <t>BLM</t> ( n = 9) groups. ** P < 0.01. B Percentages of ALDH br , CD45 − /ALDH br , CD45 − /ALDH br /EpCAM + , and CD45 − /ALDH br /PDGFRα + cells in total lung cells during BLM-induced pulmonary fibrosis ( n = 6/group). * P < 0.05, ** P < 0.01. ns, not significant. C Correlations between lung hydroxyproline content on day 14 and percentages of ALDH br , CD45 − /ALDH br , CD45 − /ALDH br /EpCAM + , and CD45 − /ALDH br /PDGFRα + cells in total lung cells. D Real-time quantitative PCR analysis of the mRNA expression levels of ALDH isoforms in the lungs obtained from the PBS ( n = 4) and BLM ( n = 9) groups on day 14. Values are expressed relative to the expression of the endogenous control β-actin mRNA. Data are shown as mean ± SEM. * P < 0.05, ** P < 0.01
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90
Jackson Laboratory c57bl/6n mice
Decreased CD45 − /ALDH br <t>during</t> <t>pulmonary</t> fibrosis. A Lung hydroxyproline content on day 14 in the PBS ( n = 4) and the <t>BLM</t> ( n = 9) groups. ** P < 0.01. B Percentages of ALDH br , CD45 − /ALDH br , CD45 − /ALDH br /EpCAM + , and CD45 − /ALDH br /PDGFRα + cells in total lung cells during BLM-induced pulmonary fibrosis ( n = 6/group). * P < 0.05, ** P < 0.01. ns, not significant. C Correlations between lung hydroxyproline content on day 14 and percentages of ALDH br , CD45 − /ALDH br , CD45 − /ALDH br /EpCAM + , and CD45 − /ALDH br /PDGFRα + cells in total lung cells. D Real-time quantitative PCR analysis of the mRNA expression levels of ALDH isoforms in the lungs obtained from the PBS ( n = 4) and BLM ( n = 9) groups on day 14. Values are expressed relative to the expression of the endogenous control β-actin mRNA. Data are shown as mean ± SEM. * P < 0.05, ** P < 0.01
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Adooq Bioscience LLC bleomycin sulfate blm
Decreased CD45 − /ALDH br <t>during</t> <t>pulmonary</t> fibrosis. A Lung hydroxyproline content on day 14 in the PBS ( n = 4) and the <t>BLM</t> ( n = 9) groups. ** P < 0.01. B Percentages of ALDH br , CD45 − /ALDH br , CD45 − /ALDH br /EpCAM + , and CD45 − /ALDH br /PDGFRα + cells in total lung cells during BLM-induced pulmonary fibrosis ( n = 6/group). * P < 0.05, ** P < 0.01. ns, not significant. C Correlations between lung hydroxyproline content on day 14 and percentages of ALDH br , CD45 − /ALDH br , CD45 − /ALDH br /EpCAM + , and CD45 − /ALDH br /PDGFRα + cells in total lung cells. D Real-time quantitative PCR analysis of the mRNA expression levels of ALDH isoforms in the lungs obtained from the PBS ( n = 4) and BLM ( n = 9) groups on day 14. Values are expressed relative to the expression of the endogenous control β-actin mRNA. Data are shown as mean ± SEM. * P < 0.05, ** P < 0.01
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clea japan inc c57bl/6n mice
Decreased CD45 − /ALDH br <t>during</t> <t>pulmonary</t> fibrosis. A Lung hydroxyproline content on day 14 in the PBS ( n = 4) and the <t>BLM</t> ( n = 9) groups. ** P < 0.01. B Percentages of ALDH br , CD45 − /ALDH br , CD45 − /ALDH br /EpCAM + , and CD45 − /ALDH br /PDGFRα + cells in total lung cells during BLM-induced pulmonary fibrosis ( n = 6/group). * P < 0.05, ** P < 0.01. ns, not significant. C Correlations between lung hydroxyproline content on day 14 and percentages of ALDH br , CD45 − /ALDH br , CD45 − /ALDH br /EpCAM + , and CD45 − /ALDH br /PDGFRα + cells in total lung cells. D Real-time quantitative PCR analysis of the mRNA expression levels of ALDH isoforms in the lungs obtained from the PBS ( n = 4) and BLM ( n = 9) groups on day 14. Values are expressed relative to the expression of the endogenous control β-actin mRNA. Data are shown as mean ± SEM. * P < 0.05, ** P < 0.01
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Dawley Inc sprague dawley rats
Overview of the research progress of Chinese herbal medicine polysaccharides in the treatment of PF.
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Overview of the research progress of Chinese herbal medicine polysaccharides in the treatment of PF.
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Image Search Results


PRDM16 was decreased in aged organs and SnCs. a) qPCR analysis of PRDM family members in the kidneys, lungs, heart and stomach of young (2 months old) and aged (24 months old) mice (n = 3). b) qPCR analysis of Prdm16 in multiple organs of 2 months mice (n = 6). c) Analysis of one published transcriptomic dataset showed that PRDM16 decreased with age in human normal renal cortex (n = 71). d–f) Tests for linear trend were conducted between age and PRDM16 mRNA level in the heart (d) (n = 384), brain hippocampus (e) (n = 187) and lung (f) (n = 345) of humans based on transcriptomes from ADEIP. g) Correlational analysis of PRDM16 mRNA level (log 10 (2 −(ΔΔCt) )) and age in human normal lung samples (n = 13). h) Correlational analysis of the mRNA levels (log 10 (2 −(ΔΔCt) )) of PRDM16 and CDKN1A in human normal lung samples (n = 13). i) qPCR analysis of Prdm16 in the kidneys, lungs, brain hippocampus and heart of 2 months old (2 M) and 24 months old (24 M) mice (n = 6). j) Representative immunohistochemical (IHC) staining images of PRDM16 in the kidney of 2 months and 24 months mice. Scale bar: 50 µm. k) Diagram detailing X‐ray radiation, BLM and DOX induced cellular senescence. l) qPCR analysis of Prdm16 in senescent HK‐2, Beas‐2B and H9C2 cells (n = 3). Data are mean ± SEM. * p < 0.05, ** p < 0.01 and *** p < 0.001. Spearman's correlations (c, g and h), Test for linear trend (d–f), Two‐tailed Student's unpaired t ‐test analysis (i and l).

Journal: Advanced Science

Article Title: PRDM16 Reduces Cellular Senescence by Upregulating GSTM1

doi: 10.1002/advs.202501233

Figure Lengend Snippet: PRDM16 was decreased in aged organs and SnCs. a) qPCR analysis of PRDM family members in the kidneys, lungs, heart and stomach of young (2 months old) and aged (24 months old) mice (n = 3). b) qPCR analysis of Prdm16 in multiple organs of 2 months mice (n = 6). c) Analysis of one published transcriptomic dataset showed that PRDM16 decreased with age in human normal renal cortex (n = 71). d–f) Tests for linear trend were conducted between age and PRDM16 mRNA level in the heart (d) (n = 384), brain hippocampus (e) (n = 187) and lung (f) (n = 345) of humans based on transcriptomes from ADEIP. g) Correlational analysis of PRDM16 mRNA level (log 10 (2 −(ΔΔCt) )) and age in human normal lung samples (n = 13). h) Correlational analysis of the mRNA levels (log 10 (2 −(ΔΔCt) )) of PRDM16 and CDKN1A in human normal lung samples (n = 13). i) qPCR analysis of Prdm16 in the kidneys, lungs, brain hippocampus and heart of 2 months old (2 M) and 24 months old (24 M) mice (n = 6). j) Representative immunohistochemical (IHC) staining images of PRDM16 in the kidney of 2 months and 24 months mice. Scale bar: 50 µm. k) Diagram detailing X‐ray radiation, BLM and DOX induced cellular senescence. l) qPCR analysis of Prdm16 in senescent HK‐2, Beas‐2B and H9C2 cells (n = 3). Data are mean ± SEM. * p < 0.05, ** p < 0.01 and *** p < 0.001. Spearman's correlations (c, g and h), Test for linear trend (d–f), Two‐tailed Student's unpaired t ‐test analysis (i and l).

Article Snippet: For BLM induced senescence research, Beas‐2B cells were treated with 6 μg mL −1 BLM (HY‐17565, MCE) for 48 h. Rat embryonic cardiomyocyte (H9C2) line was obtained from American Type Culture Collection (ATCC).

Techniques: Immunohistochemical staining, Immunohistochemistry, Two Tailed Test

The effect of Longidaze on the hematological parameters of C57BL/6 mice modeling bleomycin-induced pulmonary fibrosis on d7. Hematological parameters after pirfenidone administration per os, after intramuscular ( a ) and intranasal ( b ) administration of different doses of Longidaze. Groups of mice: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal. WBCs—white blood cells (10 9 /L blood); GRA 10 9 , LYM 10 9 , MON 10 9 (absolute number), GRA %, LYM %, MON % (relative number)—number of neutrophils, lymphocytes, monocytes; RBCs 10 12 —red blood cells (10 12 /L blood). Statistical analysis of data was performed using the Kruskal–Wallis test, post hoc Wilcoxon test for pairwise comparisons with bleomycin control group (with corresponding route of administration), and Bonferroni correction (ns— p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Journal: Life

Article Title: Anti-Inflammatory and Antifibrotic Potential of Longidaze in Bleomycin-Induced Pulmonary Fibrosis

doi: 10.3390/life13091932

Figure Lengend Snippet: The effect of Longidaze on the hematological parameters of C57BL/6 mice modeling bleomycin-induced pulmonary fibrosis on d7. Hematological parameters after pirfenidone administration per os, after intramuscular ( a ) and intranasal ( b ) administration of different doses of Longidaze. Groups of mice: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal. WBCs—white blood cells (10 9 /L blood); GRA 10 9 , LYM 10 9 , MON 10 9 (absolute number), GRA %, LYM %, MON % (relative number)—number of neutrophils, lymphocytes, monocytes; RBCs 10 12 —red blood cells (10 12 /L blood). Statistical analysis of data was performed using the Kruskal–Wallis test, post hoc Wilcoxon test for pairwise comparisons with bleomycin control group (with corresponding route of administration), and Bonferroni correction (ns— p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Article Snippet: Experimental pulmonary fibrosis was induced by a single intratracheal bleomycin (BLM, Nippon Kayaku Co., Ltd., Tokyo, Japan) administration at a dose 80 μg/mouse in 0.03 mL of 0.9% NaCl, which was slowly instilled in the tracheal lumen [ ].

Techniques:

The effect of Longidaze on the hematological parameters of C57BL/6 mice modeling bleomycin-induced pulmonary fibrosis on d21. Hematological parameters after pirfenidone administration per os, after intramuscular ( a ) and intranasal ( b ) administration of different doses of Longidaze. Groups of mice: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal. WBCs—white blood cells (10 9 /L blood); GRA 10 9 , LYM 10 9 , MON 10 9 (absolute number), GRA %, LYM %, MON % (relative number)—number of neutrophils, lymphocytes, monocytes; RBCs 10 12 —red blood cells (10 12 /L blood). Statistical analysis of data was performed using the Kruskal–Wallis test, post hoc Wilcoxon test for pairwise comparisons with bleomycin control group (with corresponding route of administration), and Bonferroni correction (ns— p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Journal: Life

Article Title: Anti-Inflammatory and Antifibrotic Potential of Longidaze in Bleomycin-Induced Pulmonary Fibrosis

doi: 10.3390/life13091932

Figure Lengend Snippet: The effect of Longidaze on the hematological parameters of C57BL/6 mice modeling bleomycin-induced pulmonary fibrosis on d21. Hematological parameters after pirfenidone administration per os, after intramuscular ( a ) and intranasal ( b ) administration of different doses of Longidaze. Groups of mice: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal. WBCs—white blood cells (10 9 /L blood); GRA 10 9 , LYM 10 9 , MON 10 9 (absolute number), GRA %, LYM %, MON % (relative number)—number of neutrophils, lymphocytes, monocytes; RBCs 10 12 —red blood cells (10 12 /L blood). Statistical analysis of data was performed using the Kruskal–Wallis test, post hoc Wilcoxon test for pairwise comparisons with bleomycin control group (with corresponding route of administration), and Bonferroni correction (ns— p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Article Snippet: Experimental pulmonary fibrosis was induced by a single intratracheal bleomycin (BLM, Nippon Kayaku Co., Ltd., Tokyo, Japan) administration at a dose 80 μg/mouse in 0.03 mL of 0.9% NaCl, which was slowly instilled in the tracheal lumen [ ].

Techniques:

Histological analysis of lung inflammation on d7. Representative photomicrographs of lung tissue sections obtained from male C57BL/6 mice and stained with H&E. ×100. Scale bar 50 μm. Groups: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal.

Journal: Life

Article Title: Anti-Inflammatory and Antifibrotic Potential of Longidaze in Bleomycin-Induced Pulmonary Fibrosis

doi: 10.3390/life13091932

Figure Lengend Snippet: Histological analysis of lung inflammation on d7. Representative photomicrographs of lung tissue sections obtained from male C57BL/6 mice and stained with H&E. ×100. Scale bar 50 μm. Groups: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal.

Article Snippet: Experimental pulmonary fibrosis was induced by a single intratracheal bleomycin (BLM, Nippon Kayaku Co., Ltd., Tokyo, Japan) administration at a dose 80 μg/mouse in 0.03 mL of 0.9% NaCl, which was slowly instilled in the tracheal lumen [ ].

Techniques: Staining

Photomicrographs of lung sections obtained from male C57BL/6 mice on d21. Tissues were stained with H&E. ×100. Scale bar 50 μm. Groups: Intact—intact control mice (group 1); Vehicle i.m. and Vehicle i.n.—bleomycin treated mice (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal.

Journal: Life

Article Title: Anti-Inflammatory and Antifibrotic Potential of Longidaze in Bleomycin-Induced Pulmonary Fibrosis

doi: 10.3390/life13091932

Figure Lengend Snippet: Photomicrographs of lung sections obtained from male C57BL/6 mice on d21. Tissues were stained with H&E. ×100. Scale bar 50 μm. Groups: Intact—intact control mice (group 1); Vehicle i.m. and Vehicle i.n.—bleomycin treated mice (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal.

Article Snippet: Experimental pulmonary fibrosis was induced by a single intratracheal bleomycin (BLM, Nippon Kayaku Co., Ltd., Tokyo, Japan) administration at a dose 80 μg/mouse in 0.03 mL of 0.9% NaCl, which was slowly instilled in the tracheal lumen [ ].

Techniques: Staining

Effect of Longidaze on perivascular and peribronchial inflammation in the lungs of C57BL/6 mice on d7. Representative images of lung tissue section stained with H&E ( a ) and its respective inflammation scores ( b ). Groups: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal. Statistical analysis of data was performed using the Kruskal–Wallis test, post hoc Wilcoxon test for pairwise comparisons with the bleomycin control group (with appropriate route of administration), and Bonferroni correction (ns— p > 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Journal: Life

Article Title: Anti-Inflammatory and Antifibrotic Potential of Longidaze in Bleomycin-Induced Pulmonary Fibrosis

doi: 10.3390/life13091932

Figure Lengend Snippet: Effect of Longidaze on perivascular and peribronchial inflammation in the lungs of C57BL/6 mice on d7. Representative images of lung tissue section stained with H&E ( a ) and its respective inflammation scores ( b ). Groups: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal. Statistical analysis of data was performed using the Kruskal–Wallis test, post hoc Wilcoxon test for pairwise comparisons with the bleomycin control group (with appropriate route of administration), and Bonferroni correction (ns— p > 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Article Snippet: Experimental pulmonary fibrosis was induced by a single intratracheal bleomycin (BLM, Nippon Kayaku Co., Ltd., Tokyo, Japan) administration at a dose 80 μg/mouse in 0.03 mL of 0.9% NaCl, which was slowly instilled in the tracheal lumen [ ].

Techniques: Staining

Effects of Longidaze on the content of connective tissue in the lungs of C57BL/6 mice on d21. ( a ) Photomicrographs of left lung sections (middle pulmonary field) obtained from male C57BL/6 mice on d21. Tissues stained by Van Gieson, scale bar 100 μm. ( b ) Content of the connective tissue in the lungs of C57BL/6 mice from all groups; ( c ) content of the connective tissue in the lungs of C57BL/6 mice from groups after intramuscularly administration; ( d ) content of the connective tissue in the lungs of C57BL/6 mice from groups after intranasal administration. Groups: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal. Statistical analysis of data was performed using the Kruskal–Wallis test, post hoc Wilcoxon test for pairwise comparisons with the bleomycin control group (with appropriate route of administration), and Bonferroni correction (ns— p > 0.05, **** p < 0.0001).

Journal: Life

Article Title: Anti-Inflammatory and Antifibrotic Potential of Longidaze in Bleomycin-Induced Pulmonary Fibrosis

doi: 10.3390/life13091932

Figure Lengend Snippet: Effects of Longidaze on the content of connective tissue in the lungs of C57BL/6 mice on d21. ( a ) Photomicrographs of left lung sections (middle pulmonary field) obtained from male C57BL/6 mice on d21. Tissues stained by Van Gieson, scale bar 100 μm. ( b ) Content of the connective tissue in the lungs of C57BL/6 mice from all groups; ( c ) content of the connective tissue in the lungs of C57BL/6 mice from groups after intramuscularly administration; ( d ) content of the connective tissue in the lungs of C57BL/6 mice from groups after intranasal administration. Groups: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal. Statistical analysis of data was performed using the Kruskal–Wallis test, post hoc Wilcoxon test for pairwise comparisons with the bleomycin control group (with appropriate route of administration), and Bonferroni correction (ns— p > 0.05, **** p < 0.0001).

Article Snippet: Experimental pulmonary fibrosis was induced by a single intratracheal bleomycin (BLM, Nippon Kayaku Co., Ltd., Tokyo, Japan) administration at a dose 80 μg/mouse in 0.03 mL of 0.9% NaCl, which was slowly instilled in the tracheal lumen [ ].

Techniques: Staining

Effects of Longidaze treatment on the IL-6, TNF-α, and hyaluronic acid levels in homogenate of right lung lobes received from male C57BL/6 mice on d7. ELISA parameters after pirfenidone administration per os, after intramuscular ( a ) and intranasal ( b ) administration of different doses of Longidaze. Groups of mice: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal. Statistical analysis of data was performed using the Kruskal–Wallis test, post hoc Wilcoxon test for pairwise comparisons with the bleomycin control group (with appropriate route of administration), and Bonferroni correction (ns— p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Journal: Life

Article Title: Anti-Inflammatory and Antifibrotic Potential of Longidaze in Bleomycin-Induced Pulmonary Fibrosis

doi: 10.3390/life13091932

Figure Lengend Snippet: Effects of Longidaze treatment on the IL-6, TNF-α, and hyaluronic acid levels in homogenate of right lung lobes received from male C57BL/6 mice on d7. ELISA parameters after pirfenidone administration per os, after intramuscular ( a ) and intranasal ( b ) administration of different doses of Longidaze. Groups of mice: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal. Statistical analysis of data was performed using the Kruskal–Wallis test, post hoc Wilcoxon test for pairwise comparisons with the bleomycin control group (with appropriate route of administration), and Bonferroni correction (ns— p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Article Snippet: Experimental pulmonary fibrosis was induced by a single intratracheal bleomycin (BLM, Nippon Kayaku Co., Ltd., Tokyo, Japan) administration at a dose 80 μg/mouse in 0.03 mL of 0.9% NaCl, which was slowly instilled in the tracheal lumen [ ].

Techniques: Enzyme-linked Immunosorbent Assay

Effects of Longidaze treatment on hyaluronic acid, collagen I, hydroxyproline, and TGF-β1 levels in right lung lobe homogenate obtained from male C57BL/6 mice on d21. ELISA parameters after pirfenidone administration per os, after intramuscular ( a ) and intranasal ( b ) administration of different doses of Longidaze. Groups of mice: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal. Statistical analysis of data was performed using the Kruskal–Wallis test, post hoc Wilcoxon test for pairwise comparisons with the bleomycin control group (with appropriate route of administration), and Bonferroni correction (ns— p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Journal: Life

Article Title: Anti-Inflammatory and Antifibrotic Potential of Longidaze in Bleomycin-Induced Pulmonary Fibrosis

doi: 10.3390/life13091932

Figure Lengend Snippet: Effects of Longidaze treatment on hyaluronic acid, collagen I, hydroxyproline, and TGF-β1 levels in right lung lobe homogenate obtained from male C57BL/6 mice on d21. ELISA parameters after pirfenidone administration per os, after intramuscular ( a ) and intranasal ( b ) administration of different doses of Longidaze. Groups of mice: Intact—mice of intact control (group 1); Vehicle i.m. and Vehicle i.n.—mice treated with bleomycin (groups 2 and 3, respectively); pirfenidone 300 mg/kg p.o.—pulmonary fibrosis + pirfenidone (group 4); LG 60 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 60 U/kg (group 5); LG 120 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 120 U/kg (group 6); LG 1200 U/kg i.m.—pulmonary fibrosis + Longidaze intramuscularly at a dose of 1200 U/kg (group 7); LG 10 U/kg i.n.—pulmonary fibrosis + Longidaze intranasally at a dose of 10 U/kg (group 8); LG 30 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 30 U/kg (group 9); LG 120 U/kg i.n.—pulmonary fibrosis + Longidaze intranasal at a dose of 120 U/kg (group 10). P.o.—per os, i.m.—intramuscular, i.n.—intranasal. Statistical analysis of data was performed using the Kruskal–Wallis test, post hoc Wilcoxon test for pairwise comparisons with the bleomycin control group (with appropriate route of administration), and Bonferroni correction (ns— p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Article Snippet: Experimental pulmonary fibrosis was induced by a single intratracheal bleomycin (BLM, Nippon Kayaku Co., Ltd., Tokyo, Japan) administration at a dose 80 μg/mouse in 0.03 mL of 0.9% NaCl, which was slowly instilled in the tracheal lumen [ ].

Techniques: Enzyme-linked Immunosorbent Assay

Decreased CD45 − /ALDH br during pulmonary fibrosis. A Lung hydroxyproline content on day 14 in the PBS ( n = 4) and the BLM ( n = 9) groups. ** P < 0.01. B Percentages of ALDH br , CD45 − /ALDH br , CD45 − /ALDH br /EpCAM + , and CD45 − /ALDH br /PDGFRα + cells in total lung cells during BLM-induced pulmonary fibrosis ( n = 6/group). * P < 0.05, ** P < 0.01. ns, not significant. C Correlations between lung hydroxyproline content on day 14 and percentages of ALDH br , CD45 − /ALDH br , CD45 − /ALDH br /EpCAM + , and CD45 − /ALDH br /PDGFRα + cells in total lung cells. D Real-time quantitative PCR analysis of the mRNA expression levels of ALDH isoforms in the lungs obtained from the PBS ( n = 4) and BLM ( n = 9) groups on day 14. Values are expressed relative to the expression of the endogenous control β-actin mRNA. Data are shown as mean ± SEM. * P < 0.05, ** P < 0.01

Journal: Stem Cell Research & Therapy

Article Title: Antifibrotic effect of lung-resident progenitor cells with high aldehyde dehydrogenase activity

doi: 10.1186/s13287-021-02549-6

Figure Lengend Snippet: Decreased CD45 − /ALDH br during pulmonary fibrosis. A Lung hydroxyproline content on day 14 in the PBS ( n = 4) and the BLM ( n = 9) groups. ** P < 0.01. B Percentages of ALDH br , CD45 − /ALDH br , CD45 − /ALDH br /EpCAM + , and CD45 − /ALDH br /PDGFRα + cells in total lung cells during BLM-induced pulmonary fibrosis ( n = 6/group). * P < 0.05, ** P < 0.01. ns, not significant. C Correlations between lung hydroxyproline content on day 14 and percentages of ALDH br , CD45 − /ALDH br , CD45 − /ALDH br /EpCAM + , and CD45 − /ALDH br /PDGFRα + cells in total lung cells. D Real-time quantitative PCR analysis of the mRNA expression levels of ALDH isoforms in the lungs obtained from the PBS ( n = 4) and BLM ( n = 9) groups on day 14. Values are expressed relative to the expression of the endogenous control β-actin mRNA. Data are shown as mean ± SEM. * P < 0.05, ** P < 0.01

Article Snippet: On day 0, after intraperitoneal injection of mixed anesthesia with medetomidine hydrochloride (0.3 mg/kg body weight; Kyoritsu Seiyaku, Tokyo, Japan), midazolam (4 mg/kg body weight, Sandoz K.K., Tokyo, Japan), and butorphanol tartrate (5 mg/kg body weight, Meiji Seika Pharma, Tokyo, Japan), pulmonary fibrosis was induced by endotracheal injection of BLM (2 mg/kg of body weight, Nippon Kayaku, Tokyo, Japan).

Techniques: Real-time Polymerase Chain Reaction, Expressing

CD45 − /ALDH br cell therapy ameliorates BLM-induced pulmonary fibrosis CD45 − /ALDH br cell therapy ameliorates BLM-induced pulmonary fibrosis. A Lung hydroxyproline content on day 14 in BLM-treated mice transferred with CD45 − /ALDH dim ( n = 7) and CD45 − /ALDH br ( n = 4) cells on day 2. * P < 0.05. B HE-staining of lung tissue sections obtained from PBS-treated and BLM-treated mice transferred with CD45 − /ALDH dim and CD45 − /ALDH br cells. C Real-time quantitative PCR analysis of the mRNA expression levels of TGF-β1 and IL-6 in lung tissues on day 7 obtained from BLM-treated mice transferred with CD45 − /ALDH dim ( n = 9–10) and CD45 − /ALDH br ( n = 7–8) cells. Values are expressed relative to the expression of the endogenous control β-actin mRNA and normalized to the mean value of the CD45 − /ALDH dim i.v. group set as 1. * P < 0.05. D Representative images of flow cytometry of lung CD45 − /ALDH br cells in BLM-treated mice transferred with PBS alone, CD45 − /ALDH dim cells, and CD45 − /ALDH br cells on day 14. E Real-time quantitative PCR analysis of the mRNA expression levels of ALDH isoforms in the lungs obtained from BLM-treated mice transferred with CD45 − /ALDH dim ( n = 7) and CD45 − /ALDH br ( n = 4) cells on day 14. Values are expressed relative to the expression of endogenous control β-actin mRNA. Data are shown as mean ± SEM. * P < 0.05. F Schematic summary of the retinol-metabolizing pathway. Circulating retinol/vitamin A is taken up into a cell via the cell membrane receptor (stimulated by retinoic acid 6, STRA6). It is converted into retinal/retinaldehyde within the cytoplasm, which is further converted into all-trans-retinoic acid (ATRA) by retinal dehydrogenase/retinaldehyde dehydrogenase (RALDH, ALDH1a family). Subsequently, it is transported into the nucleus by the cellular retinoic acid-binding protein (CRABP), where ATRA binds to the intranuclear retinoic acid receptor (RAR) and promotes gene transcription. G Real-time quantitative PCR analysis of the mRNA expression levels of retinol-metabolizing pathway-related genes in the lung tissues obtained from BLM-treated mice transferred with CD45 − /ALDH dim ( n = 7) and CD45 − /ALDH br ( n = 4) cells on day 14. Values are expressed relative to the expression of the endogenous control β-actin mRNA. Data are shown as mean ± SEM. * P < 0.05. (H) Survival rate in high-dose BLM-treated mice transferred with PBS alone ( n = 8), CD45 − /ALDH dim ( n = 8) cells, and CD45 − /ALDH br ( n = 5) cells

Journal: Stem Cell Research & Therapy

Article Title: Antifibrotic effect of lung-resident progenitor cells with high aldehyde dehydrogenase activity

doi: 10.1186/s13287-021-02549-6

Figure Lengend Snippet: CD45 − /ALDH br cell therapy ameliorates BLM-induced pulmonary fibrosis CD45 − /ALDH br cell therapy ameliorates BLM-induced pulmonary fibrosis. A Lung hydroxyproline content on day 14 in BLM-treated mice transferred with CD45 − /ALDH dim ( n = 7) and CD45 − /ALDH br ( n = 4) cells on day 2. * P < 0.05. B HE-staining of lung tissue sections obtained from PBS-treated and BLM-treated mice transferred with CD45 − /ALDH dim and CD45 − /ALDH br cells. C Real-time quantitative PCR analysis of the mRNA expression levels of TGF-β1 and IL-6 in lung tissues on day 7 obtained from BLM-treated mice transferred with CD45 − /ALDH dim ( n = 9–10) and CD45 − /ALDH br ( n = 7–8) cells. Values are expressed relative to the expression of the endogenous control β-actin mRNA and normalized to the mean value of the CD45 − /ALDH dim i.v. group set as 1. * P < 0.05. D Representative images of flow cytometry of lung CD45 − /ALDH br cells in BLM-treated mice transferred with PBS alone, CD45 − /ALDH dim cells, and CD45 − /ALDH br cells on day 14. E Real-time quantitative PCR analysis of the mRNA expression levels of ALDH isoforms in the lungs obtained from BLM-treated mice transferred with CD45 − /ALDH dim ( n = 7) and CD45 − /ALDH br ( n = 4) cells on day 14. Values are expressed relative to the expression of endogenous control β-actin mRNA. Data are shown as mean ± SEM. * P < 0.05. F Schematic summary of the retinol-metabolizing pathway. Circulating retinol/vitamin A is taken up into a cell via the cell membrane receptor (stimulated by retinoic acid 6, STRA6). It is converted into retinal/retinaldehyde within the cytoplasm, which is further converted into all-trans-retinoic acid (ATRA) by retinal dehydrogenase/retinaldehyde dehydrogenase (RALDH, ALDH1a family). Subsequently, it is transported into the nucleus by the cellular retinoic acid-binding protein (CRABP), where ATRA binds to the intranuclear retinoic acid receptor (RAR) and promotes gene transcription. G Real-time quantitative PCR analysis of the mRNA expression levels of retinol-metabolizing pathway-related genes in the lung tissues obtained from BLM-treated mice transferred with CD45 − /ALDH dim ( n = 7) and CD45 − /ALDH br ( n = 4) cells on day 14. Values are expressed relative to the expression of the endogenous control β-actin mRNA. Data are shown as mean ± SEM. * P < 0.05. (H) Survival rate in high-dose BLM-treated mice transferred with PBS alone ( n = 8), CD45 − /ALDH dim ( n = 8) cells, and CD45 − /ALDH br ( n = 5) cells

Article Snippet: On day 0, after intraperitoneal injection of mixed anesthesia with medetomidine hydrochloride (0.3 mg/kg body weight; Kyoritsu Seiyaku, Tokyo, Japan), midazolam (4 mg/kg body weight, Sandoz K.K., Tokyo, Japan), and butorphanol tartrate (5 mg/kg body weight, Meiji Seika Pharma, Tokyo, Japan), pulmonary fibrosis was induced by endotracheal injection of BLM (2 mg/kg of body weight, Nippon Kayaku, Tokyo, Japan).

Techniques: Staining, Real-time Polymerase Chain Reaction, Expressing, Flow Cytometry, Binding Assay

Effect of aging on ALDH activity. A Percentages of CD45 − /ALDH br and CD45 − /ALDH br /PDGFRα + cells in total lung cells during BLM-induced pulmonary fibrosis in young and aged mice ( n = 4–6). * P < 0.05, ** P < 0.01. ns, not significant. B ALDH activity in primary cultured lung fibroblasts obtained from young and aged mice ( n = 5–10) before and 7 days after treatment with BLM. ** P < 0.01. ns, not significant

Journal: Stem Cell Research & Therapy

Article Title: Antifibrotic effect of lung-resident progenitor cells with high aldehyde dehydrogenase activity

doi: 10.1186/s13287-021-02549-6

Figure Lengend Snippet: Effect of aging on ALDH activity. A Percentages of CD45 − /ALDH br and CD45 − /ALDH br /PDGFRα + cells in total lung cells during BLM-induced pulmonary fibrosis in young and aged mice ( n = 4–6). * P < 0.05, ** P < 0.01. ns, not significant. B ALDH activity in primary cultured lung fibroblasts obtained from young and aged mice ( n = 5–10) before and 7 days after treatment with BLM. ** P < 0.01. ns, not significant

Article Snippet: On day 0, after intraperitoneal injection of mixed anesthesia with medetomidine hydrochloride (0.3 mg/kg body weight; Kyoritsu Seiyaku, Tokyo, Japan), midazolam (4 mg/kg body weight, Sandoz K.K., Tokyo, Japan), and butorphanol tartrate (5 mg/kg body weight, Meiji Seika Pharma, Tokyo, Japan), pulmonary fibrosis was induced by endotracheal injection of BLM (2 mg/kg of body weight, Nippon Kayaku, Tokyo, Japan).

Techniques: Activity Assay, Cell Culture

Overview of the research progress of Chinese herbal medicine polysaccharides in the treatment of PF.

Journal: Frontiers in Pharmacology

Article Title: Multi-Pharmaceutical Activities of Chinese Herbal Polysaccharides in the Treatment of Pulmonary Fibrosis: Concept and Future Prospects

doi: 10.3389/fphar.2021.707491

Figure Lengend Snippet: Overview of the research progress of Chinese herbal medicine polysaccharides in the treatment of PF.

Article Snippet: PDO , Man:Glc = 5.9:1, it is composed of (1→4)-linked Man and (1→4)-linked Glc , 1.78 × 10 5 Da , (1→4)-linked Man (1→4)-connected Glc , In vivo : BLM induced adult male Sprague Dawley rats. In vitro : TGF-β1 induced type II alveolar epithelial cells (RLE-6TN, CRL-2300) , PDO can reduce the number of neutrophils in rat lung tissue induced by BLM, improve inflammation and fibrosis, enhance Smad2/3 and inhibit the expression of pSmad2/3 protein through TGFβ1, thereby inhibiting the type II rat alveolar epithelial cells (RLE-6TN, CRL-2300) induced by TGF-β1 fibronectin and COL-1 , ( ; ; ; ; ) .

Techniques: In Vivo, In Vitro, Phospho-proteomics, Expressing, Sequencing, Residue, Modification, Glycoproteomics, Activity Assay