Fig. 3

BMSCs alleviate the activation of HSCs after hypoxia–reoxygenation and reduce apoptosis, but do not affect their proliferation. (A) Flowchart of BMSCs co-culturing with HSC-T6 cells after hypoxia–reoxygenation. (B) Western blot analyses of COL1A1, MMP9, DES, TGFB1, ACTA2, and TIMP1 in HSC-T6 cells. TUBA1A was used as the loading control. Col1a1, Mmp9, Des, Tgfb1, Acta2, and Timp1 mRNA levels in HSC-T6 cells. (C) Microscopic images of each group stained with EDU staining (magnification: ×200, n = 3). (D) Apoptosis results of flow cytometry in each group. Cell cycle results of flow cytometry in each group. Full-length blots/gels are presented in Supplementary Fig. 2. The samples were derived from the same experiment and processed in parallel. ACTA2, actin alpha 2; BMSCs, bone mesenchymal stem cells; COL1A1, collagen type I alpha 1 chain; DES, desmin; EDU, 5-Ethynyl-2’-deoxyuridine; HSCs, hepatic stellate cells; MMP9, matrix metalloproteinase 9; TGFB1, transforming growth factor beta 1; TIMP1, tissue inhibitor of metalloproteinase 1. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001