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: In addition, the hydroxyproline (HYP) content of mouse lung tissues were measured to quantify lung collagen contents and determined colourimetrically with a hydroxyproline assay kit (KGT030-2, KeyGen Biotech, Nanjing, China) following the manufacturer's instructions.

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

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: In addition, the hydroxyproline (HYP) content of mouse lung tissues were measured to quantify lung collagen contents and determined colourimetrically with a hydroxyproline assay kit (KGT030-2, KeyGen Biotech, Nanjing, China) following the manufacturer's instructions.

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

Journal: Frontiers in Pharmacology

Article Title: Marine-derived surfactin derivatives suppress collagen production and interfere with the HSP47-collagen interaction in preclinical models

doi: 10.3389/fphar.2026.1809175

Figure Lengend Snippet: Antifibrotic properties of surfactin in mouse lung fibrotic models. (A) Western blot analysis of type I collagen in mouse lung fibroblasts treated with surfactin. Mlg cells (1.5 × 10 5 ) were seeded into six-well plates, cultured overnight, and treated with surfactin at concentrations of 10, 30, or 100 μM or with vehicle control for 2 d. Type I collagen expression was analyzed by Western blotting and normalized to GAPDH. Data represent mean ± standard deviation from four independent experiments. Statistical significance was determined using one-way ANOVA with multiple comparisons (***p < 0.001). (B) Quantification of lung hydroxyproline content. C57BL/6 mice received intratracheal bleomycin (1.5 mg/kg). Beginning the following day, mice were administered surfactin (200 mg/kg) or vehicle by daily oral gavage. Mice were euthanized on day 21 for the collection of BAL and lung tissue. The right lungs were homogenized, and hydroxyproline content was determined and normalized to lung weight (mg/g). (C,D) BAL cell counts and total protein concentration. BAL fluid was centrifuged, and supernatants were analyzed for protein concentration using the BCA assay. Cell pellets were resuspended in PBS for total cell counting. Data represent mean ± standard deviation. Statistical significance was determined using the Student’s t-test (*p < 0.05). (E) Histological assessment of the left lungs by Masson’s trichrome staining. Representative images in each group are shown. GAPDH, glyceraldehyde 3-phosphate dehydrogenase; PBS, phosphate-buffered saline; BCA, bicinchoninic acid assay; BAL, bronchoalveolar lavage; Mlg, mouse lung fibroblasts.

Article Snippet: Hydroxyproline content in homogenized right lungs was measured using a hydroxyproline assay kit (QuickZyme Biosciences B.V., Leiden, Netherlands) according to the manufacturer’s instructions.

Techniques: Western Blot, Cell Culture, Control, Expressing, Standard Deviation, Protein Concentration, BIA-KA, Cell Counting, Staining, Saline, Acid Assay