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    Structured Review

    Proteintech collagen i
    FoxM1 is highly expressed in fibroblasts of fibrotic lung tissues. (A, B) qPCR (n = 9) and Western blot (n = 6) analysis of the expression of FoxM1 in normal and IPF lung tissues. ∗ P < 0.05. (C) qPCR analysis of the mRNA levels of FoxM1 in the lung tissues from BLM-treated mice. n = 3, ∗ P < 0.05. (D) Western blot analysis of the protein levels of FoxM1, CTHRC1, α-SMA, and <t>Collagen</t> <t>I</t> in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) The Pearson's correlation analysis of COL1A1 expression with FoxM1 expression based on the RNA-seq results of GSE24206 from GEO database. (F) The Pearson's correlation analysis of Ashcroft score with FoxM1 expression in the lung tissues from BLM-treated mice. (G) Representative images of co-immunostaining for α-SMA and FoxM1 in IPF lung tissues. White arrows indicate double-positive cells. (H) Representative images of co-immunostaining for α-SMA and FoxM1 in the lung tissues from BLM-treated mice. White arrows indicate double-positive cells. (I) Western blot analysis of FoxM1 expression in pulmonary fibroblasts isolated from mice subjected to BLM treatment. n = 3, ∗ P < 0.05. (J) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TGF-β1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A, B, I) and one-way ANOVA with Tukey's post-hoc test (C, D, J) were used for statistical analysis.
    Collagen I, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 788 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+collagen+type+i/Collagen+Type+I+Antibody/pmc12991958-77-14-16
    Average 96 stars, based on 788 article reviews
    collagen i - by Bioz Stars, 2026-09
    96/100 stars

    Images

    1) Product Images from "SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts"

    Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

    Journal: Redox Biology

    doi: 10.1016/j.redox.2026.104108

    FoxM1 is highly expressed in fibroblasts of fibrotic lung tissues. (A, B) qPCR (n = 9) and Western blot (n = 6) analysis of the expression of FoxM1 in normal and IPF lung tissues. ∗ P < 0.05. (C) qPCR analysis of the mRNA levels of FoxM1 in the lung tissues from BLM-treated mice. n = 3, ∗ P < 0.05. (D) Western blot analysis of the protein levels of FoxM1, CTHRC1, α-SMA, and Collagen I in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) The Pearson's correlation analysis of COL1A1 expression with FoxM1 expression based on the RNA-seq results of GSE24206 from GEO database. (F) The Pearson's correlation analysis of Ashcroft score with FoxM1 expression in the lung tissues from BLM-treated mice. (G) Representative images of co-immunostaining for α-SMA and FoxM1 in IPF lung tissues. White arrows indicate double-positive cells. (H) Representative images of co-immunostaining for α-SMA and FoxM1 in the lung tissues from BLM-treated mice. White arrows indicate double-positive cells. (I) Western blot analysis of FoxM1 expression in pulmonary fibroblasts isolated from mice subjected to BLM treatment. n = 3, ∗ P < 0.05. (J) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TGF-β1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A, B, I) and one-way ANOVA with Tukey's post-hoc test (C, D, J) were used for statistical analysis.
    Figure Legend Snippet: FoxM1 is highly expressed in fibroblasts of fibrotic lung tissues. (A, B) qPCR (n = 9) and Western blot (n = 6) analysis of the expression of FoxM1 in normal and IPF lung tissues. ∗ P < 0.05. (C) qPCR analysis of the mRNA levels of FoxM1 in the lung tissues from BLM-treated mice. n = 3, ∗ P < 0.05. (D) Western blot analysis of the protein levels of FoxM1, CTHRC1, α-SMA, and Collagen I in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) The Pearson's correlation analysis of COL1A1 expression with FoxM1 expression based on the RNA-seq results of GSE24206 from GEO database. (F) The Pearson's correlation analysis of Ashcroft score with FoxM1 expression in the lung tissues from BLM-treated mice. (G) Representative images of co-immunostaining for α-SMA and FoxM1 in IPF lung tissues. White arrows indicate double-positive cells. (H) Representative images of co-immunostaining for α-SMA and FoxM1 in the lung tissues from BLM-treated mice. White arrows indicate double-positive cells. (I) Western blot analysis of FoxM1 expression in pulmonary fibroblasts isolated from mice subjected to BLM treatment. n = 3, ∗ P < 0.05. (J) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TGF-β1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A, B, I) and one-way ANOVA with Tukey's post-hoc test (C, D, J) were used for statistical analysis.

    Techniques Used: Western Blot, Expressing, RNA Sequencing, Immunostaining, Isolation

    Impairing nuclear translocation of FoxM1 suppresses fibroblast activation and protects mice from bleomycin-induced pulmonary fibrosis. (A) Western blot analysis was performed to assess the nuclear expression levels of FoxM1 in pulmonary fibroblasts isolated from BLM-treated mice. n = 3, ∗ P < 0.05. (B) Western blot analysis of nuclear FoxM1, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (C, D) EdU assay for the proliferation of TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (E) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from BLM-treated mice injected with or without RCM-1. (F, G) The ashcroft score (n = 6, ∗ P < 0.05.) and hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of BLM-treated mice injected with or without RCM-1. (H) The survival of BLM-treated mice injected with or without RCM-1. n = 18. (I) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in the lung tissues from BLM-treated mice injected with or without RCM-1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A) and one-way ANOVA with Tukey's post-hoc test (B, D, F–I) were used for statistical analysis.
    Figure Legend Snippet: Impairing nuclear translocation of FoxM1 suppresses fibroblast activation and protects mice from bleomycin-induced pulmonary fibrosis. (A) Western blot analysis was performed to assess the nuclear expression levels of FoxM1 in pulmonary fibroblasts isolated from BLM-treated mice. n = 3, ∗ P < 0.05. (B) Western blot analysis of nuclear FoxM1, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (C, D) EdU assay for the proliferation of TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (E) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from BLM-treated mice injected with or without RCM-1. (F, G) The ashcroft score (n = 6, ∗ P < 0.05.) and hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of BLM-treated mice injected with or without RCM-1. (H) The survival of BLM-treated mice injected with or without RCM-1. n = 18. (I) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in the lung tissues from BLM-treated mice injected with or without RCM-1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A) and one-way ANOVA with Tukey's post-hoc test (B, D, F–I) were used for statistical analysis.

    Techniques Used: Translocation Assay, Activation Assay, Western Blot, Expressing, Isolation, EdU Assay, Staining, Injection

    Acetylation of FoxM1 is required for the activation of pulmonary fibroblasts. (A, B) Western blot analysis of FoxM1 expression in the cytoplasm and nucleus of CHX-treated pulmonary fibroblasts along with or without MG132 treatment at indicated time. n = 3, ∗ P < 0.05. (C) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts along with or without TGF-β1 treatment. n = 3, ∗ P < 0.05. (D) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts isolated from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts treated with or without TGF-β1. n = 3, ∗ P < 0.05. (F, G) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TSA (50 nM), or NAM (1 mM) for 24 h, or not. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (D, E) and one-way ANOVA with Tukey's post-hoc test (B, C, G) were used for statistical analysis.
    Figure Legend Snippet: Acetylation of FoxM1 is required for the activation of pulmonary fibroblasts. (A, B) Western blot analysis of FoxM1 expression in the cytoplasm and nucleus of CHX-treated pulmonary fibroblasts along with or without MG132 treatment at indicated time. n = 3, ∗ P < 0.05. (C) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts along with or without TGF-β1 treatment. n = 3, ∗ P < 0.05. (D) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts isolated from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts treated with or without TGF-β1. n = 3, ∗ P < 0.05. (F, G) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TSA (50 nM), or NAM (1 mM) for 24 h, or not. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (D, E) and one-way ANOVA with Tukey's post-hoc test (B, C, G) were used for statistical analysis.

    Techniques Used: Activation Assay, Western Blot, Expressing, Isolation

    Sirt3-dependent deacetylation of FoxM1 regulates the stability of FoxM1. (A) The Pearson's correlation analysis of COL1A1 expression with SIRTs expression based on the RNA-seq results of GSE2052 from GEO database. (B) Western blot analysis of SIRT3 expression in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (C) Western blot analysis of the acetylation levels of FoxM1 in SIRT3 flox/flox mice intratracheally injected with AAV-Cre. n = 3, ∗ P < 0.05. (D) Western blot analysis was performed to assess the acetylation status of FoxM1 in pulmonary fibroblasts following transfection with Sirt3 siRNA (si-Sirt3). n = 3, ∗ P < 0.05. (E) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, α-SMA and Collagen I expression in pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (G) EdU assay for the proliferation of pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (H) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts transfected with or without LV-Sirt3. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (B-D, F, G) and one-way ANOVA with Tukey's post-hoc test (E, H) were used for statistical analysis.
    Figure Legend Snippet: Sirt3-dependent deacetylation of FoxM1 regulates the stability of FoxM1. (A) The Pearson's correlation analysis of COL1A1 expression with SIRTs expression based on the RNA-seq results of GSE2052 from GEO database. (B) Western blot analysis of SIRT3 expression in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (C) Western blot analysis of the acetylation levels of FoxM1 in SIRT3 flox/flox mice intratracheally injected with AAV-Cre. n = 3, ∗ P < 0.05. (D) Western blot analysis was performed to assess the acetylation status of FoxM1 in pulmonary fibroblasts following transfection with Sirt3 siRNA (si-Sirt3). n = 3, ∗ P < 0.05. (E) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, α-SMA and Collagen I expression in pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (G) EdU assay for the proliferation of pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (H) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts transfected with or without LV-Sirt3. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (B-D, F, G) and one-way ANOVA with Tukey's post-hoc test (E, H) were used for statistical analysis.

    Techniques Used: Expressing, RNA Sequencing, Western Blot, Injection, Transfection, EdU Assay

    Sirt3 knockdown accelerates BLM-induced pulmonary fibrosis via activation pulmonary fibroblasts in vivo. (A) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from SIRT3 flox/flox mice or BLM-treated SIRT3 flox/flox mice that intratracheally injected with or without AAV-Cre. (B, C) The ashcroft score (n = 6, ∗ P < 0.05.) and the hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of mice treated as in A. (D) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in A n = 3, ∗ P < 0.05. (E) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from mice treated as in A n = 3, ∗ P < 0.05. (F, G) EdU assay for the proliferation of pulmonary fibroblasts isolated from mice treated as in A. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.
    Figure Legend Snippet: Sirt3 knockdown accelerates BLM-induced pulmonary fibrosis via activation pulmonary fibroblasts in vivo. (A) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from SIRT3 flox/flox mice or BLM-treated SIRT3 flox/flox mice that intratracheally injected with or without AAV-Cre. (B, C) The ashcroft score (n = 6, ∗ P < 0.05.) and the hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of mice treated as in A. (D) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in A n = 3, ∗ P < 0.05. (E) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from mice treated as in A n = 3, ∗ P < 0.05. (F, G) EdU assay for the proliferation of pulmonary fibroblasts isolated from mice treated as in A. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.

    Techniques Used: Knockdown, Activation Assay, In Vivo, Staining, Injection, Western Blot, Expressing, Isolation, EdU Assay

    Nicotinamide riboside protects mice from bleomycin-induced pulmonary fibrosis via activation of SIRT3. (A) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without NR treatment. n = 3, ∗ P < 0.05. (B) Cell viability assessment using the CCK-8 assay in pulmonary fibroblasts treated as in A n = 6, ∗ P < 0.05. (C) The survival of BLM-treated mice oral gavaged with or without NR. n = 18. (D) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from mice treated as in C. (E) The ashcroft score of mice treated as in C n = 6, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in C n = 3, ∗ P < 0.05. (G) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from the lung tissues of mice treated as in C n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.
    Figure Legend Snippet: Nicotinamide riboside protects mice from bleomycin-induced pulmonary fibrosis via activation of SIRT3. (A) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without NR treatment. n = 3, ∗ P < 0.05. (B) Cell viability assessment using the CCK-8 assay in pulmonary fibroblasts treated as in A n = 6, ∗ P < 0.05. (C) The survival of BLM-treated mice oral gavaged with or without NR. n = 18. (D) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from mice treated as in C. (E) The ashcroft score of mice treated as in C n = 6, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in C n = 3, ∗ P < 0.05. (G) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from the lung tissues of mice treated as in C n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.

    Techniques Used: Activation Assay, Western Blot, Expressing, CCK-8 Assay, Staining, Isolation

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    Membrane:

    Article Title: H3K18 lactylation-hexokinase 2 positive feedback loop promotes osteogenesis of ASPCs in facial infiltrating lipomatosis.
    Article Snippet: The proteins were combined with a protein sample buffer (Epizyme, LT101) in a ratio of 4:1, and then subjected to a heat treatment at 100 °C for 7 min prior to being resolved on 0.45 μm PVDF membranes. .. After a 15-minute blocking step with a Protein Free Rapid Blocking Buffer (1×) (Epizyme, PS108P), the membrane was incubated overnight with primary antibodies, including pan anti-kla (PTM Bio, PTM-1401RM), anti-H3K18la (PTM Bio, PTM-1427RM), anti-H3K9la (PTM Bio, PTM-1419RM), anti-H3K23la (PTM Bio, PTM-1413RM), anti-H4K5la (PTM Bio, PTM-1407RM), anti-H4K12la (PTM Bio, PTM-1411RM), anti-α tubulin (Proteintech, 11224-1-AP), anti-HK2 (Epizyme, R010880), anti-LDHA (Cell Signaling Technology, 2012), anti-Histone H3 (HUABIO, M1309-1), anti-Histone H4 (HUABIO, ET1612-43), anti-LDHB (Cell Signaling Technology, 56298), anti-RUNX2 (Proteintech, 20700- 1-AP), anti-Collagen type I (COL-1, Proteintech, 67288- 1-Ig), anti-ALP (Abcam, ab307726), anti-PPAR γ (Cell Signaling Technology, 2443 S), anti-C/EBP α (Proteintech, 13274-1-AP), and anti-FABP 4 (Proteintech, 12802- 1-AP) overnight. .. Subsequently, the membranes were incubated with secondary antibodies for 45 min at room temperature and visualized using NcmECL Ultra (NCM Biotech, Suzhou, China) with the Tanon 4600 Automatic Chemiluminescence/Fluorescence Image Analysis System (Tanon, Shanghai, China).

    Article Title: H3K18 lactylation-hexokinase 2 positive feedback loop promotes osteogenesis of ASPCs in facial infiltrating lipomatosis
    Article Snippet: The proteins were combined with a protein sample buffer (Epizyme, LT101) in a ratio of 4:1, and then subjected to a heat treatment at 100 °C for 7 min prior to being resolved on 0.45 μm PVDF membranes. .. After a 15-minute blocking step with a Protein Free Rapid Blocking Buffer (1×) (Epizyme, PS108P), the membrane was incubated overnight with primary antibodies, including pan anti-kla (PTM Bio, PTM-1401RM), anti-H3K18la (PTM Bio, PTM-1427RM), anti-H3K9la (PTM Bio, PTM-1419RM), anti-H3K23la (PTM Bio, PTM-1413RM), anti-H4K5la (PTM Bio, PTM-1407RM), anti-H4K12la (PTM Bio, PTM-1411RM), anti-α tubulin (Proteintech, 11224-1-AP), anti-HK2 (Epizyme, R010880), anti-LDHA (Cell Signaling Technology, 2012), anti-Histone H3 (HUABIO, M1309-1), anti-Histone H4 (HUABIO, ET1612-43), anti-LDHB (Cell Signaling Technology, 56298), anti-RUNX2 (Proteintech, 20700-1-AP), anti-Collagen type I (COL-1, Proteintech, 67288-1-Ig), anti-ALP (Abcam, ab307726), anti-PPAR γ (Cell Signaling Technology, 2443 S), anti-C/EBP α (Proteintech, 13274-1-AP), and anti-FABP 4 (Proteintech, 12802-1-AP) overnight. .. Subsequently, the membranes were incubated with secondary antibodies for 45 min at room temperature and visualized using NcmECL Ultra (NCM Biotech, Suzhou, China) with the Tanon 4600 Automatic Chemiluminescence/Fluorescence Image Analysis System (Tanon, Shanghai, China).

    Incubation:

    Article Title: H3K18 lactylation-hexokinase 2 positive feedback loop promotes osteogenesis of ASPCs in facial infiltrating lipomatosis.
    Article Snippet: The proteins were combined with a protein sample buffer (Epizyme, LT101) in a ratio of 4:1, and then subjected to a heat treatment at 100 °C for 7 min prior to being resolved on 0.45 μm PVDF membranes. .. After a 15-minute blocking step with a Protein Free Rapid Blocking Buffer (1×) (Epizyme, PS108P), the membrane was incubated overnight with primary antibodies, including pan anti-kla (PTM Bio, PTM-1401RM), anti-H3K18la (PTM Bio, PTM-1427RM), anti-H3K9la (PTM Bio, PTM-1419RM), anti-H3K23la (PTM Bio, PTM-1413RM), anti-H4K5la (PTM Bio, PTM-1407RM), anti-H4K12la (PTM Bio, PTM-1411RM), anti-α tubulin (Proteintech, 11224-1-AP), anti-HK2 (Epizyme, R010880), anti-LDHA (Cell Signaling Technology, 2012), anti-Histone H3 (HUABIO, M1309-1), anti-Histone H4 (HUABIO, ET1612-43), anti-LDHB (Cell Signaling Technology, 56298), anti-RUNX2 (Proteintech, 20700- 1-AP), anti-Collagen type I (COL-1, Proteintech, 67288- 1-Ig), anti-ALP (Abcam, ab307726), anti-PPAR γ (Cell Signaling Technology, 2443 S), anti-C/EBP α (Proteintech, 13274-1-AP), and anti-FABP 4 (Proteintech, 12802- 1-AP) overnight. .. Subsequently, the membranes were incubated with secondary antibodies for 45 min at room temperature and visualized using NcmECL Ultra (NCM Biotech, Suzhou, China) with the Tanon 4600 Automatic Chemiluminescence/Fluorescence Image Analysis System (Tanon, Shanghai, China).

    Article Title: Hybrid methacrylated PCL/inulin photosensitive resins for 3D printing: a step forward in bone tissue engineering.
    Article Snippet: .. Cells were then incubated overnight at 4 1C with rabbit polyclonal primary antibodies diluted in blocking buffer: anti-osteocalcin (OCN, Merck; 1 : 200) and anti-collagen type I (Coll I, Proteintech; 1 : 200). ..

    Article Title: H3K18 lactylation-hexokinase 2 positive feedback loop promotes osteogenesis of ASPCs in facial infiltrating lipomatosis
    Article Snippet: The proteins were combined with a protein sample buffer (Epizyme, LT101) in a ratio of 4:1, and then subjected to a heat treatment at 100 °C for 7 min prior to being resolved on 0.45 μm PVDF membranes. .. After a 15-minute blocking step with a Protein Free Rapid Blocking Buffer (1×) (Epizyme, PS108P), the membrane was incubated overnight with primary antibodies, including pan anti-kla (PTM Bio, PTM-1401RM), anti-H3K18la (PTM Bio, PTM-1427RM), anti-H3K9la (PTM Bio, PTM-1419RM), anti-H3K23la (PTM Bio, PTM-1413RM), anti-H4K5la (PTM Bio, PTM-1407RM), anti-H4K12la (PTM Bio, PTM-1411RM), anti-α tubulin (Proteintech, 11224-1-AP), anti-HK2 (Epizyme, R010880), anti-LDHA (Cell Signaling Technology, 2012), anti-Histone H3 (HUABIO, M1309-1), anti-Histone H4 (HUABIO, ET1612-43), anti-LDHB (Cell Signaling Technology, 56298), anti-RUNX2 (Proteintech, 20700-1-AP), anti-Collagen type I (COL-1, Proteintech, 67288-1-Ig), anti-ALP (Abcam, ab307726), anti-PPAR γ (Cell Signaling Technology, 2443 S), anti-C/EBP α (Proteintech, 13274-1-AP), and anti-FABP 4 (Proteintech, 12802-1-AP) overnight. .. Subsequently, the membranes were incubated with secondary antibodies for 45 min at room temperature and visualized using NcmECL Ultra (NCM Biotech, Suzhou, China) with the Tanon 4600 Automatic Chemiluminescence/Fluorescence Image Analysis System (Tanon, Shanghai, China).

    Article Title: Hypoxia Induces HIF-1α Activation in Tendon Stem Cells to Enhance Extracellular Vesicle-Mediated Tendon Repair.
    Article Snippet: Tendon injuries are challenging to treat due to the limited blood supply and low cell density in tendon tissue.. Tendon stem cells (TSCs) typically reside in a hypoxic environment (1%−5% oxygen), which may be crucial for their physiological function.. In this study, we demonstrated that under hypoxic conditions, TSCs release small extracellular vesicles (sEVs) enriched with functional molecules (mainly noncoding RNAs and proteins).



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    (A) Representative Hematoxylin & eosin (H&E) staining images of wound sections; The red arrow refers to the skin appendage. (B) Representative Masson’s trichrome staining images of wound sections; blue color indicates collagen. (C) Representative immunohistochemical images of wound sections showing type-I collagen (COLI) expression. (D) Representative immunohistochemical images of wound sections showing type-III collagen (COLIII) expression. (E) Quantification of total collagen deposition (Masson-stained area %). (F) Quantification of COLI deposition (% positively stained area). (G) Quantification of COLIII deposition (% positively stained area). In E–G, data are mean ± SD from three independent animals (n = 3 mice per group). Statistical significance was evaluated by one-way ANOVA and LSD comparison test. Ns, no significant difference (P > 0.05); *P < 0.05, **P < 0.01, ***P < 0.001.

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    Article Title: A bioactive hydrogel integrating bFGF/VEGFA gene-loaded nanoparticles and platelet-rich plasma for accelerated full-thickness skin wound healing

    doi: 10.1371/journal.pone.0350087

    Figure Lengend Snippet: (A) Representative Hematoxylin & eosin (H&E) staining images of wound sections; The red arrow refers to the skin appendage. (B) Representative Masson’s trichrome staining images of wound sections; blue color indicates collagen. (C) Representative immunohistochemical images of wound sections showing type-I collagen (COLI) expression. (D) Representative immunohistochemical images of wound sections showing type-III collagen (COLIII) expression. (E) Quantification of total collagen deposition (Masson-stained area %). (F) Quantification of COLI deposition (% positively stained area). (G) Quantification of COLIII deposition (% positively stained area). In E–G, data are mean ± SD from three independent animals (n = 3 mice per group). Statistical significance was evaluated by one-way ANOVA and LSD comparison test. Ns, no significant difference (P > 0.05); *P < 0.05, **P < 0.01, ***P < 0.001.

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    Techniques: Staining, Immunohistochemical staining, Expressing, Comparison

    FoxM1 is highly expressed in fibroblasts of fibrotic lung tissues. (A, B) qPCR (n = 9) and Western blot (n = 6) analysis of the expression of FoxM1 in normal and IPF lung tissues. ∗ P < 0.05. (C) qPCR analysis of the mRNA levels of FoxM1 in the lung tissues from BLM-treated mice. n = 3, ∗ P < 0.05. (D) Western blot analysis of the protein levels of FoxM1, CTHRC1, α-SMA, and Collagen I in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) The Pearson's correlation analysis of COL1A1 expression with FoxM1 expression based on the RNA-seq results of GSE24206 from GEO database. (F) The Pearson's correlation analysis of Ashcroft score with FoxM1 expression in the lung tissues from BLM-treated mice. (G) Representative images of co-immunostaining for α-SMA and FoxM1 in IPF lung tissues. White arrows indicate double-positive cells. (H) Representative images of co-immunostaining for α-SMA and FoxM1 in the lung tissues from BLM-treated mice. White arrows indicate double-positive cells. (I) Western blot analysis of FoxM1 expression in pulmonary fibroblasts isolated from mice subjected to BLM treatment. n = 3, ∗ P < 0.05. (J) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TGF-β1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A, B, I) and one-way ANOVA with Tukey's post-hoc test (C, D, J) were used for statistical analysis.

    Journal: Redox Biology

    Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

    doi: 10.1016/j.redox.2026.104108

    Figure Lengend Snippet: FoxM1 is highly expressed in fibroblasts of fibrotic lung tissues. (A, B) qPCR (n = 9) and Western blot (n = 6) analysis of the expression of FoxM1 in normal and IPF lung tissues. ∗ P < 0.05. (C) qPCR analysis of the mRNA levels of FoxM1 in the lung tissues from BLM-treated mice. n = 3, ∗ P < 0.05. (D) Western blot analysis of the protein levels of FoxM1, CTHRC1, α-SMA, and Collagen I in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) The Pearson's correlation analysis of COL1A1 expression with FoxM1 expression based on the RNA-seq results of GSE24206 from GEO database. (F) The Pearson's correlation analysis of Ashcroft score with FoxM1 expression in the lung tissues from BLM-treated mice. (G) Representative images of co-immunostaining for α-SMA and FoxM1 in IPF lung tissues. White arrows indicate double-positive cells. (H) Representative images of co-immunostaining for α-SMA and FoxM1 in the lung tissues from BLM-treated mice. White arrows indicate double-positive cells. (I) Western blot analysis of FoxM1 expression in pulmonary fibroblasts isolated from mice subjected to BLM treatment. n = 3, ∗ P < 0.05. (J) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TGF-β1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A, B, I) and one-way ANOVA with Tukey's post-hoc test (C, D, J) were used for statistical analysis.

    Article Snippet: The primary antibodies used were: FoxM1, α-SMA, SIRT3 and Lamin B1 (Selleckchem, Houston, USA), Collagen I (Proteintech, Wuhan, China) and GAPDH (ABclonal, Wuhan, China).

    Techniques: Western Blot, Expressing, RNA Sequencing, Immunostaining, Isolation

    Impairing nuclear translocation of FoxM1 suppresses fibroblast activation and protects mice from bleomycin-induced pulmonary fibrosis. (A) Western blot analysis was performed to assess the nuclear expression levels of FoxM1 in pulmonary fibroblasts isolated from BLM-treated mice. n = 3, ∗ P < 0.05. (B) Western blot analysis of nuclear FoxM1, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (C, D) EdU assay for the proliferation of TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (E) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from BLM-treated mice injected with or without RCM-1. (F, G) The ashcroft score (n = 6, ∗ P < 0.05.) and hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of BLM-treated mice injected with or without RCM-1. (H) The survival of BLM-treated mice injected with or without RCM-1. n = 18. (I) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in the lung tissues from BLM-treated mice injected with or without RCM-1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A) and one-way ANOVA with Tukey's post-hoc test (B, D, F–I) were used for statistical analysis.

    Journal: Redox Biology

    Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

    doi: 10.1016/j.redox.2026.104108

    Figure Lengend Snippet: Impairing nuclear translocation of FoxM1 suppresses fibroblast activation and protects mice from bleomycin-induced pulmonary fibrosis. (A) Western blot analysis was performed to assess the nuclear expression levels of FoxM1 in pulmonary fibroblasts isolated from BLM-treated mice. n = 3, ∗ P < 0.05. (B) Western blot analysis of nuclear FoxM1, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (C, D) EdU assay for the proliferation of TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (E) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from BLM-treated mice injected with or without RCM-1. (F, G) The ashcroft score (n = 6, ∗ P < 0.05.) and hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of BLM-treated mice injected with or without RCM-1. (H) The survival of BLM-treated mice injected with or without RCM-1. n = 18. (I) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in the lung tissues from BLM-treated mice injected with or without RCM-1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A) and one-way ANOVA with Tukey's post-hoc test (B, D, F–I) were used for statistical analysis.

    Article Snippet: The primary antibodies used were: FoxM1, α-SMA, SIRT3 and Lamin B1 (Selleckchem, Houston, USA), Collagen I (Proteintech, Wuhan, China) and GAPDH (ABclonal, Wuhan, China).

    Techniques: Translocation Assay, Activation Assay, Western Blot, Expressing, Isolation, EdU Assay, Staining, Injection

    Acetylation of FoxM1 is required for the activation of pulmonary fibroblasts. (A, B) Western blot analysis of FoxM1 expression in the cytoplasm and nucleus of CHX-treated pulmonary fibroblasts along with or without MG132 treatment at indicated time. n = 3, ∗ P < 0.05. (C) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts along with or without TGF-β1 treatment. n = 3, ∗ P < 0.05. (D) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts isolated from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts treated with or without TGF-β1. n = 3, ∗ P < 0.05. (F, G) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TSA (50 nM), or NAM (1 mM) for 24 h, or not. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (D, E) and one-way ANOVA with Tukey's post-hoc test (B, C, G) were used for statistical analysis.

    Journal: Redox Biology

    Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

    doi: 10.1016/j.redox.2026.104108

    Figure Lengend Snippet: Acetylation of FoxM1 is required for the activation of pulmonary fibroblasts. (A, B) Western blot analysis of FoxM1 expression in the cytoplasm and nucleus of CHX-treated pulmonary fibroblasts along with or without MG132 treatment at indicated time. n = 3, ∗ P < 0.05. (C) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts along with or without TGF-β1 treatment. n = 3, ∗ P < 0.05. (D) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts isolated from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts treated with or without TGF-β1. n = 3, ∗ P < 0.05. (F, G) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TSA (50 nM), or NAM (1 mM) for 24 h, or not. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (D, E) and one-way ANOVA with Tukey's post-hoc test (B, C, G) were used for statistical analysis.

    Article Snippet: The primary antibodies used were: FoxM1, α-SMA, SIRT3 and Lamin B1 (Selleckchem, Houston, USA), Collagen I (Proteintech, Wuhan, China) and GAPDH (ABclonal, Wuhan, China).

    Techniques: Activation Assay, Western Blot, Expressing, Isolation

    Sirt3-dependent deacetylation of FoxM1 regulates the stability of FoxM1. (A) The Pearson's correlation analysis of COL1A1 expression with SIRTs expression based on the RNA-seq results of GSE2052 from GEO database. (B) Western blot analysis of SIRT3 expression in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (C) Western blot analysis of the acetylation levels of FoxM1 in SIRT3 flox/flox mice intratracheally injected with AAV-Cre. n = 3, ∗ P < 0.05. (D) Western blot analysis was performed to assess the acetylation status of FoxM1 in pulmonary fibroblasts following transfection with Sirt3 siRNA (si-Sirt3). n = 3, ∗ P < 0.05. (E) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, α-SMA and Collagen I expression in pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (G) EdU assay for the proliferation of pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (H) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts transfected with or without LV-Sirt3. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (B-D, F, G) and one-way ANOVA with Tukey's post-hoc test (E, H) were used for statistical analysis.

    Journal: Redox Biology

    Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

    doi: 10.1016/j.redox.2026.104108

    Figure Lengend Snippet: Sirt3-dependent deacetylation of FoxM1 regulates the stability of FoxM1. (A) The Pearson's correlation analysis of COL1A1 expression with SIRTs expression based on the RNA-seq results of GSE2052 from GEO database. (B) Western blot analysis of SIRT3 expression in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (C) Western blot analysis of the acetylation levels of FoxM1 in SIRT3 flox/flox mice intratracheally injected with AAV-Cre. n = 3, ∗ P < 0.05. (D) Western blot analysis was performed to assess the acetylation status of FoxM1 in pulmonary fibroblasts following transfection with Sirt3 siRNA (si-Sirt3). n = 3, ∗ P < 0.05. (E) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, α-SMA and Collagen I expression in pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (G) EdU assay for the proliferation of pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (H) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts transfected with or without LV-Sirt3. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (B-D, F, G) and one-way ANOVA with Tukey's post-hoc test (E, H) were used for statistical analysis.

    Article Snippet: The primary antibodies used were: FoxM1, α-SMA, SIRT3 and Lamin B1 (Selleckchem, Houston, USA), Collagen I (Proteintech, Wuhan, China) and GAPDH (ABclonal, Wuhan, China).

    Techniques: Expressing, RNA Sequencing, Western Blot, Injection, Transfection, EdU Assay

    Sirt3 knockdown accelerates BLM-induced pulmonary fibrosis via activation pulmonary fibroblasts in vivo. (A) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from SIRT3 flox/flox mice or BLM-treated SIRT3 flox/flox mice that intratracheally injected with or without AAV-Cre. (B, C) The ashcroft score (n = 6, ∗ P < 0.05.) and the hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of mice treated as in A. (D) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in A n = 3, ∗ P < 0.05. (E) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from mice treated as in A n = 3, ∗ P < 0.05. (F, G) EdU assay for the proliferation of pulmonary fibroblasts isolated from mice treated as in A. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.

    Journal: Redox Biology

    Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

    doi: 10.1016/j.redox.2026.104108

    Figure Lengend Snippet: Sirt3 knockdown accelerates BLM-induced pulmonary fibrosis via activation pulmonary fibroblasts in vivo. (A) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from SIRT3 flox/flox mice or BLM-treated SIRT3 flox/flox mice that intratracheally injected with or without AAV-Cre. (B, C) The ashcroft score (n = 6, ∗ P < 0.05.) and the hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of mice treated as in A. (D) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in A n = 3, ∗ P < 0.05. (E) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from mice treated as in A n = 3, ∗ P < 0.05. (F, G) EdU assay for the proliferation of pulmonary fibroblasts isolated from mice treated as in A. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.

    Article Snippet: The primary antibodies used were: FoxM1, α-SMA, SIRT3 and Lamin B1 (Selleckchem, Houston, USA), Collagen I (Proteintech, Wuhan, China) and GAPDH (ABclonal, Wuhan, China).

    Techniques: Knockdown, Activation Assay, In Vivo, Staining, Injection, Western Blot, Expressing, Isolation, EdU Assay

    Nicotinamide riboside protects mice from bleomycin-induced pulmonary fibrosis via activation of SIRT3. (A) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without NR treatment. n = 3, ∗ P < 0.05. (B) Cell viability assessment using the CCK-8 assay in pulmonary fibroblasts treated as in A n = 6, ∗ P < 0.05. (C) The survival of BLM-treated mice oral gavaged with or without NR. n = 18. (D) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from mice treated as in C. (E) The ashcroft score of mice treated as in C n = 6, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in C n = 3, ∗ P < 0.05. (G) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from the lung tissues of mice treated as in C n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.

    Journal: Redox Biology

    Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

    doi: 10.1016/j.redox.2026.104108

    Figure Lengend Snippet: Nicotinamide riboside protects mice from bleomycin-induced pulmonary fibrosis via activation of SIRT3. (A) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without NR treatment. n = 3, ∗ P < 0.05. (B) Cell viability assessment using the CCK-8 assay in pulmonary fibroblasts treated as in A n = 6, ∗ P < 0.05. (C) The survival of BLM-treated mice oral gavaged with or without NR. n = 18. (D) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from mice treated as in C. (E) The ashcroft score of mice treated as in C n = 6, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in C n = 3, ∗ P < 0.05. (G) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from the lung tissues of mice treated as in C n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.

    Article Snippet: The primary antibodies used were: FoxM1, α-SMA, SIRT3 and Lamin B1 (Selleckchem, Houston, USA), Collagen I (Proteintech, Wuhan, China) and GAPDH (ABclonal, Wuhan, China).

    Techniques: Activation Assay, Western Blot, Expressing, CCK-8 Assay, Staining, Isolation

    Results of antioxidant and pro-collagen effects of CA-PDENs. (A) Graphical depiction of DPPH radical scavenging activity of CA-PDENs and vitamin C within the concentration of 6.25-400 µg/mL, data are presented as mean ± standard deviation (n = 3). (B) Fluorescence intensity in UVB-induced 1BR3 cells represents the level of intracellular ROS after CA-PDENs treatment for 24 hours; data are presented as mean ± standard deviation (n = 3). *p < 0.05, **p-value < 0.01 vs. negative control. (C) Confocal microscopy images showing collagen type I expression in 1BR3 cells after 6 hours of CA-PDENs incubation at the concentrations of 40 and 100 µg/mL (200× magnification). Nuclei were stained with DAPI (blue), while collagen type 1 was labeled with Alexa Fluor 647 (red). Merged images show the localization of collagen type 1 expression in the cytoplasmic region surrounding the nuclei. (D) Collagen type I levels in UVB-induced 1BR3 cells followed by CA-PDENs incubation at 40 and 100 µg/mL for 48 hours, data are presented as mean ± standard deviation (n = 3). **p-value < 0.01 vs. control. Abbreviations: CA-PDENs, Centella asiatica -derived exosome-like nanovesicles; DPPH, 2,2-diphenyl-1-picrylhydrazyl; ROS, reactive oxygen species; UVB, ultraviolet B; DAPI, 4′,6-diamidino-2-phenylindole.

    Journal: Future Science OA

    Article Title: The potential of plant-derived exosome-like nanovesicles from Centella asiatica leaves (CA-PDENs) for anti-inflammation and prevention of UVB-induced photoaging

    doi: 10.1080/20565623.2026.2654777

    Figure Lengend Snippet: Results of antioxidant and pro-collagen effects of CA-PDENs. (A) Graphical depiction of DPPH radical scavenging activity of CA-PDENs and vitamin C within the concentration of 6.25-400 µg/mL, data are presented as mean ± standard deviation (n = 3). (B) Fluorescence intensity in UVB-induced 1BR3 cells represents the level of intracellular ROS after CA-PDENs treatment for 24 hours; data are presented as mean ± standard deviation (n = 3). *p < 0.05, **p-value < 0.01 vs. negative control. (C) Confocal microscopy images showing collagen type I expression in 1BR3 cells after 6 hours of CA-PDENs incubation at the concentrations of 40 and 100 µg/mL (200× magnification). Nuclei were stained with DAPI (blue), while collagen type 1 was labeled with Alexa Fluor 647 (red). Merged images show the localization of collagen type 1 expression in the cytoplasmic region surrounding the nuclei. (D) Collagen type I levels in UVB-induced 1BR3 cells followed by CA-PDENs incubation at 40 and 100 µg/mL for 48 hours, data are presented as mean ± standard deviation (n = 3). **p-value < 0.01 vs. control. Abbreviations: CA-PDENs, Centella asiatica -derived exosome-like nanovesicles; DPPH, 2,2-diphenyl-1-picrylhydrazyl; ROS, reactive oxygen species; UVB, ultraviolet B; DAPI, 4′,6-diamidino-2-phenylindole.

    Article Snippet: Cells were incubated overnight at 4 °C with a mouse anti-collagen type I primary antibody (1:500 in 1% BSA; Invitrogen, USA), followed by incubation with an Alexa Fluor 647-conjugated goat anti-mouse IgG secondary antibody (1:500 in 1% BSA; Abcam, USA) for 60 minutes in the dark.

    Techniques: Activity Assay, Concentration Assay, Standard Deviation, Fluorescence, Negative Control, Confocal Microscopy, Expressing, Incubation, Staining, Labeling, Control, Derivative Assay