blm induced senescence research Search Results


blm induced senescence research  (MedChemExpress)
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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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bleomycin  (Hexal AG)
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Hexal AG bleomycin
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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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