Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: The hypothetical pathway of this study. All the important molecular and pathways were indicated. Briefly, AMPK is a preferential substrate of Compound C than Akt in normal conditions. When TiO₂ NZs were added to cells, they inhibited the expression of AMPK and mTOR proteins, then with extra addition of Compound C or phenformin turned to inhibit the candidate target of Akt, and exerted contrary effects on regulating autophagy

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Expressing

Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: Contrasted effects of Compound C and phenformin on TiO₂ NZs–induced fetal growth impairment and placental cell energy/autophagy responses. ( A ) Representative fetal images and corresponding average fetal length and average fetal weight in the control, TiO₂ NZs, TiO₂ NZs + phenformin, and TiO₂ NZs + Compound C groups. ( B ) Immunofluorescence analysis of autophagy levels in HTR cells following exposure to 100 µg/mL TiO₂ NZs or 100 µg/mL bulk-TiO₂. ( C ) Corresponding cellular ATP levels measured after exposure to TiO₂ NZs and bulk-TiO₂. ( D - E ) Immunofluorescence analysis of autophagy levels following exposure to 100 µg/mL TiO₂ NZs or 100 µg/mL b-TiO₂, either alone or in combination with Compound C/phenformin. Cell nuclei were stained blue with DAPI, and autophagosomes were labeled red using CY3-conjugated secondary antibodies.Scale bar = 20 μm. ( F ) Uptake and location of TiO₂ NZs in HTR-8/Svneo (HTR) cells observed by TEM after cells were treated with 100 µg/mL of TiO₂ NZs. The TiO₂ NZs were indicated by red arrows. ( G ) The morphology of mitochondria observed by TEM after cells were exposed to 100 µg/mL of TiO₂ NZs. Normal or swollen mitochondria were indicated by red arrows, respectively. Data are expressed as mean ± SD. A one-way ANOVA was conducted, followed by a post-hoc Tukey’s multiple comparison test for ( A ). One-way ANOVA was used for ( C ). ** P < 0.01, *** P < 0.001 vs. control group; $ P < 0.05 TiO₂ NZs + phenformin vs. TiO₂ NZs group; # P < 0.05 TiO₂ NZs + Compound C vs. TiO₂ NZs group

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Control, Immunofluorescence, Staining, Labeling, Comparison

Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: Autophagosome accumulation and its modulation by Compound C and phenformin in placental cells. ( A - C ) Cell autophagy levels were assessed by immunofluorescence and observed using a confocal microscope after cells received corresponding treatments. ( D , E ) Cell autophagy levels were assessed by immunofluorescence after HTR cells were treated with Compound C and phenformin in the absence of TiO₂ NZs. ( F ) Autophagy levels were examined after Compound C was added to the starvation-induced autophagy group. Cell nuclei were stained with DAPI (blue), and autophagosomes were labeled with CY3-conjugated secondary antibodies (red). Scale bar = 100 μm

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Immunofluorescence, Microscopy, Staining, Labeling

Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: Compound C and phenformin differentially regulate AMPK/mTOR signaling and exhibit distinct binding modes to AKT1.( A ) Western blot analysis of AMPK, p-AMPK, mTOR, and p-mTOR expression levels in cells treated with 100 µg/mL TiO₂ NZs. ( B ) Western blot analysis of AMPK and p-AMPK expression levels in cells treated with TiO₂ NZs, either alone or in combination with Compound C or phenformin. ( C , D ) Western blot analysis of AMPK and p-AMPK expression levels in cells treated with Compound C ( C ) and phenformin ( D ). GAPDH served as a loading control. Molecular weights (kDa) are indicated beside the bands.Quantitative densitometric analysis corresponding to the western blots in ( A – D ) was performed using ImageJ software. All bands were normalized to GAPDH expression, and the tests were repeated three times. ( E ) Chemical structures of ATP-competitive AKT1 inhibitors. ( F ) Chemical structures of allosteric (auto-inhibitory) AKT1 inhibitors. ( G ) Docking conformation of Compound C at the interface of the AKT1 dimer, with AKT1a and AKT1b colored red and blue, respectively. ( H ) Docking conformation of the AKT inhibitor (4EJN) in AKT1. ( I ) Docking conformation of phenformin within the AKT1 binding site. ( J ) Superimposed binding modes of Compound C and phenformin in the AKT1 dimer. ( K, L ) Molecular docking results showing the overlapping binding region (blue frame) of Compound C and phenformin, with the upper interaction site specific to Compound C. ( M ) Docking scores (kcal/mol) of phenformin and Compound C bound to AKT1, where more negative values indicate stronger binding affinity.The data are presented as mean ± SD. An unpaired two-tailed t -test was used for ( A , C and D ). A one-way ANOVA was conducted, followed by a post-hoc Tukey’s multiple comparison test for (B). ** P < 0.01, *** P < 0.001 vs. control group; ### P < 0.001 vs. TiO₂ NZs group

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Binding Assay, Western Blot, Expressing, Control, Software, Two Tailed Test, Comparison

Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: Akt-targeted autophagy modulation emerges as AMPK declines in TiO₂ NZs-treated cells. ( A ) Western blot analysis of Akt and p-Akt protein levels in cells treated with 100 µg/mL TiO₂ NZs for 24 h. ( B, C ) Protein levels of Akt and p-Akt after treatment with Compound C or phenformin. ( D, E )Western blot analysis of Akt, p-Akt, mTOR, and p-mTOR in cells treated with TiO₂ NZs alone or in combination with Compound C or phenformin for 24 h. GAPDH served as a loading control. Molecular weights (kDa) are indicated beside the bands.Quantitative densitometric analysis corresponding to the western blots in ( A – E ) was performed using ImageJ software. All bands were normalized to GAPDH expression, and the tests were repeated three times. ( F ) AMPK mRNA and protein expression levels in cells transfected with AMPK siRNA or negative control. ( G ) Immunofluorescence analysis of autophagy levels in cells transfected with AMPK siRNA alone or in combination with Compound C or phenformin. ( H ) AMPK mRNA and protein expression levels in cells transfected with AMPK overexpression vector (pcDNA3.1-AMPK) or negative control vector (pcDNA3.1). All data are presented as the mean ± SD from three independent experiments. An unpaired two-tailed t-test was used for ( A - C ). A one-way ANOVA was conducted, followed by a post-hoc Tukey’s multiple comparison test for ( D , E , F , H ). * P < 0.05, ** P < 0.01, *** P < 0.001 vs. control group; ## P < 0.01, ### P < 0.001 vs. TiO₂ NZs group

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Western Blot, Control, Software, Expressing, Transfection, Negative Control, Immunofluorescence, Over Expression, Plasmid Preparation, Two Tailed Test, Comparison

Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: Autophagy reversal via AMPK overexpression and Akt knockdown highlights dual-target mechanism. ( A , B ) Immunofluorescence analysis of autophagy levels in HTR cells exposed to the following treatments: ( A ) Control cells, TiO₂ NZs, TiO₂ NZs + AMPK overexpression vector (pcDNA3.1-AMPK), TiO₂ NZs + AMPK overexpression vector + Compound C, or TiO₂ NZs + Compound C; ( B ) Control cells, TiO₂ NZs, TiO₂ NZs + AMPK overexpression vector, TiO₂ NZs + AMPK overexpression vector + phenformin, or TiO₂ NZs + phenformin. Cell nuclei were stained blue with DAPI, and autophagosomes were labeled red using CY3-conjugated secondary antibodies. Scale bar = 100 μm. ( C ) AKT mRNA and protein levels examined by RT-PCR and western blotting after cells were transfected with the Akt siRNA and the negative control. ( D ) Immunofluorescence analysis of autophagy levels in HTR cells exposed to the following treatments: TiO₂ NZs, TiO₂ NZs + Akt siRNA, TiO₂ NZs + Akt siRNA + Compound C, TiO₂ NZs + Compound C, TiO₂ NZs + Akt siRNA + phenformin, or TiO₂ NZs + phenformin for 24 h. Cell nuclei were stained blue with DAPI, and autophagosomes were labeled red using CY3-conjugated secondary antibodies. All data are presented as the mean ± SD. A one-way ANOVA was conducted, followed by a post-hoc Tukey’s multiple comparison test for ( C ). **** P < 0.0001 vs. NC siRNA group

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Over Expression, Knockdown, Immunofluorescence, Control, Plasmid Preparation, Staining, Labeling, Reverse Transcription Polymerase Chain Reaction, Western Blot, Transfection, Negative Control, Comparison

Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: Phenformin and Compound C rewire AMPK/mTOR pathway in HTR cells post-TiO₂ exposure. ( A, B ) Western blot analysis of Akt, AMPK, mTOR, and their phosphorylated forms after cells were treated with 100 µg/mL TiO₂ NZs, TiO₂ NZs + AMPK overexpression vector (pcDNA3.1-AMPK), or TiO₂ NZs + AMPK overexpression vector + Compound C/phenformin for 24 h. ( C ) Protein levels of AKT, p-AKT, AMPK, p-AMPK, mTOR, p-mTOR, and LC3 in the control group, TiO₂ NZs exposure group, TiO₂ NZs + phenformin and TiO₂ NZs + Compound C groups, as determined by western blotting. GAPDH served as a loading control. Molecular weights (kDa) are indicated beside the bands. Quantitative densitometric analysis corresponding to the western blots in ( A – C ) was performed using ImageJ software. All bands were normalized to GAPDH expression, and the tests were repeated three times.Data were collected from three independent experiments and presented as mean ± SD. An unpaired two-tailed t -test was used for (C left panel). A one-way ANOVA was conducted, followed by a post-hoc Tukey’s multiple comparison test for ( A , B , C right panel). * P < 0.05, ** P < 0.01, *** P < 0.001 vs. control group; # P < 0.05, ## P < 0.01, ### P < 0.001 TiO₂ NZs + AMPK-vector + Compound C vs. TiO₂ NZs group; $ P < 0.05, $$ P < 0.01, $$$ P < 0.001 TiO₂ NZs + AMPK-vector vs. TiO₂ NZs group; † P < 0.05, †† P < 0.01, ††† P < 0.001 TiO₂ NZs + AMPK-vector + Compound C vs. TiO₂ NZs + AMPK-vector group (A-B). * P < 0.05, ** P < 0.01, *** P < 0.001 vs. control group; # P < 0.05, ### P < 0.001 TiO₂ NZs + Compound C vs. TiO₂ NZs group; $ P < 0.05, $$ P < 0.01, $$$ P < 0.001 TiO₂ NZs + phenformin vs. TiO₂ NZs group ( C )

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Western Blot, Over Expression, Plasmid Preparation, Control, Software, Expressing, Two Tailed Test, Comparison

Journal: Experimental & Molecular Medicine

Article Title: Regulation of PKM2 expression and function by GLIS3 during metabolic reprogramming in polycystic kidneys

doi: 10.1038/s12276-026-01676-5

Figure Lengend Snippet: a , Representative images comparing whole kidney size between Glis3-KO2 kidneys treated with vehicle or compound 3K are shown. b , Violin plot depicting the KW/BW ratio (%) for WT and Glis3 -KO2 mice treated with vehicle or compound 3K. n ≥ 10; **** P < 0.0001. c , Representative hematoxylin and eosin-scanned images of kidney sections from Glis3 -KO2 kidneys treated with vehicle or compound 3K. Bars indicate 1 mm. d , Comparison of cystic index between Glis3 -KO2 kidneys treated with vehicle or compound 3K. Cystic index represents the percentage of renal tissue occupied by cysts. Data are presented as mean ± s.e.m., n = 6 . ** P < 0.01. e , Comparison of renal cyst size (mm 2 ) between kidneys from Glis3 -KO2 mice treated with vehicle or compound 3K. Data are presented as mean ± s.e.m., n = 6; * P < 0.05. f , Comparison of the number of cysts per kidney section between Glis3 -KO2 kidneys treated with vehicle or compound 3K. Data are presented as mean ± s.e.m., n = 8; ** P < 0.01. g , Comparison of serum creatinine levels (mg/dl) between WT and Glis3 -KO2 mice treated with vehicle or compound 3K. h , RT–qPCR analysis of Pkm2 , c-Myc , Hk2 , Havcr1 and Lcn2 between WT and Glis3 -KO2 mice treated with vehicle or compound 3K. Data are presented as mean ± s.e.m., n ≥ 5; **** P < 0.0001; *** P < 0.001; ** P < 0.01; * P < 0.05. i , Schematic illustration depicting the relationship between loss of GLIS3 function, regulation of PKM2 and cystogenesis. GLIS3 deficiency enhances Pkm gene expression in kidneys with a preferential increase in the Pkm2 isoform. Increased PKM2 phosphorylation at S37 and Y105 promotes dimer formation. PKM2-S37 phosphorylation is facilitated by increased pERK1/2 levels. Together, these events promote glycolysis, cell proliferation and cystogenesis in GLIS3-deficient kidneys. Figure 6i was created using BioRender.com.

Article Snippet: To examine the effect of PKM2 inhibition on cyst formation, PND7 Glis3 -Pax8Cre mice were treated intraperitoneally with the PKM2 inhibitor, compound 3K (S8616; Selleckchem Chemicals) (10 mg/kg) or vehicle control (10% dimethylsulfoxide (DMSO), 90% corn oil) every 24 h for 7 days.

Techniques: Comparison, Quantitative RT-PCR, Gene Expression, Phospho-proteomics

Journal: Experimental & Molecular Medicine

Article Title: Regulation of PKM2 expression and function by GLIS3 during metabolic reprogramming in polycystic kidneys

doi: 10.1038/s12276-026-01676-5

Figure Lengend Snippet: a , Immunoblot analysis of PKM2 protein levels in WT and Glis3 -KO2 RECS 3 days after siRNA-mediated PKM2-KD. Protein expression was quantified by densitometric analysis. Data are presented as mean ± s.e.m., n = 5; *** P < 0.001; ** P < 0.01. b , Analysis of lactate production in media from primary WT and Glis3 -KO2 RECs with or without PKM2-KD. c , Glycolytic rate was measured in primary WT and Glis3 -KO2 REC mice with or without PKM2-KD using a Seahorse analyzer after sequential injections of rotenone/antimycin A and 2-DG. d , e , Basal ( d ) and compensatory ( e ) glycolysis were calculated and plotted ( n = 3). f , Representative images of WT and Glis3 -KO2 REC spheroids with and without PKM2-KD at 5 and 9 days. Bars indicate 50 μm. g , Violin plot showing the size (µm) distribution of the spheroids generated at day 5 from WT and Glis3 -KO2 RECs with or without PKM2-KD ( n ≥ 4). Each data point represents an individual spheroid measurement. * P < 0.05, ** P < 0.01, *** P < 0.001. h , Spheroid images at day 5 were taken using the EVOS M7000, and spheroid diameter and number were analyzed using ImageJ and plotted according to size distribution—either 30–50, 50–100 or >100 μm. Total indicates the number of spheroids analyzed in each group ( n = 39–164). i , Violin plot showing the size (µm) distribution of the spheroids generated at day 9 from WT and Glis3 -KO2 REC mice with or without PKM2-KD ( n ≥ 4). Each data point represents an individual spheroid measurement. * P < 0.05, ** P < 0.01, *** P < 0.001. j , Day 10 spheroid size distribution—either 30–50, 50–100 or >100 μm. Total indicates the number of spheroids analyzed in each group ( n = 60–191). k , Representative image of the size of WT and Glis3 -KO2 REC spheroids 5 days following treatment with vehicle (0.1% DMSO) or compound 3K (1 μM). Bars indicate 50 μm. l , Violin plot showing the size (µm) distribution of the spheroids generated from the RECs of WT and Glis3 -KO2 kidneys ( n ≥ 4). Each data point represents an individual spheroid measurement. **** P < 0.0001. m , Size distribution—30–50, 50–100 or >100 μm of WT and Glis3 -KO2 REC spheroids with or without PKM2 inhibition. Total indicates the number of spheroids analyzed in each group (n = 39–164).

Article Snippet: To examine the effect of PKM2 inhibition on cyst formation, PND7 Glis3 -Pax8Cre mice were treated intraperitoneally with the PKM2 inhibitor, compound 3K (S8616; Selleckchem Chemicals) (10 mg/kg) or vehicle control (10% dimethylsulfoxide (DMSO), 90% corn oil) every 24 h for 7 days.

Techniques: Western Blot, Expressing, Generated, Inhibition

Journal: International journal of environmental research and public health

Article Title: A Muscarinic Antagonist Reduces Airway Inflammation and Bronchoconstriction Induced by Ambient Particulate Matter in a Mouse Model of Asthma.

doi: 10.3390/ijerph15061189

Figure Lengend Snippet: Figure 1. Experimental protocol of the mouse model of ovalbumin (OVA)-induced asthma used in the present study. For details, please see the text. FORM, formoterol fumarate; FP, fluticasone propionate; NS, normal saline; PM, particulate matter; TIO, tiotropium bromide.

Article Snippet: To investigate the effect of drugs on airway inflammation and respiratory function, mice were treated with fluticasone propionate (Toronto Research Chemicals Inc., North York, ON, Canada), formoterol fumarate (Toronto Research Chemicals Inc.), or tiotropium bromide (Tokyo Chemical Industry Co., Ltd., Tokyo, Japan) on days 21 to 26.

Techniques: Saline

Journal: International journal of environmental research and public health

Article Title: A Muscarinic Antagonist Reduces Airway Inflammation and Bronchoconstriction Induced by Ambient Particulate Matter in a Mouse Model of Asthma.

doi: 10.3390/ijerph15061189

Figure Lengend Snippet: Figure 5. Effects of fluticasone propionate, formoterol fumarate, and tiotropium bromide on airway resistance. Airway resistance was evaluated by specific airway resistance (sRaw) values on day 27. Formoterol fumarate and tiotropium bromide decreased the sRaw values compared with fluticasone propionate. Data for each group are expressed as the mean ± standard deviation, with eight mice per group. * p < 0.05.

Article Snippet: To investigate the effect of drugs on airway inflammation and respiratory function, mice were treated with fluticasone propionate (Toronto Research Chemicals Inc., North York, ON, Canada), formoterol fumarate (Toronto Research Chemicals Inc.), or tiotropium bromide (Tokyo Chemical Industry Co., Ltd., Tokyo, Japan) on days 21 to 26.

Techniques: Standard Deviation

Journal: International journal of environmental research and public health

Article Title: A Muscarinic Antagonist Reduces Airway Inflammation and Bronchoconstriction Induced by Ambient Particulate Matter in a Mouse Model of Asthma.

doi: 10.3390/ijerph15061189

Figure Lengend Snippet: Figure 6. The levels of reactive oxygen metabolites after the administration of fluticasone propionate, formoterol fumarate, and tiotropium bromide. The levels of reactive oxygen metabolites (dROMs) in serum samples obtained on day 27. Fluticasone propionate and tiotropium bromide had no effect on dROM levels compared with the control group, but formoterol fumarate increased dROM levels. Data for each group are expressed as the mean ± standard deviation, with eight mice per group. * p < 0.05.

Article Snippet: To investigate the effect of drugs on airway inflammation and respiratory function, mice were treated with fluticasone propionate (Toronto Research Chemicals Inc., North York, ON, Canada), formoterol fumarate (Toronto Research Chemicals Inc.), or tiotropium bromide (Tokyo Chemical Industry Co., Ltd., Tokyo, Japan) on days 21 to 26.

Techniques: Control, Standard Deviation