Fig. 6

The JAK1 agonist RO8191 reverses the function of BMSCs in alleviating liver fibrosis and attenuating HSCs activation. (A) Microscopic images of each group stained with HE, Masson, Sirius Red, and ACTA2 (magnification: ×100, n = 6). Area stained with Masson, Sirius Red, and ACTA2, as well as Metavir fibrosis staging. The levels of serum ALT, AST, and TBil in each group. (B) Western blot analyses of COL1A1, JAK1, p-STAT5, STAT5, ACTA2, and CASP3 in liver tissues. TUBA1A was used as the loading control except for p-STAT5. STAT5 was used as the loading control for p-STAT5. Col1a1, Jak1, Acta2, and Casp3 mRNA levels in liver tissues. (C) Western blot analyses of COL1A1, JAK1, p-STAT5, STAT5, ACTA2, and CASP3 in HSC-T6 cells. TUBA1A was used as the loading control except for p-STAT5. STAT5 was used as the loading control for p-STAT5. Col1a1, Jak1, Acta2, and Casp3 mRNA levels in HSC-T6 cells. (D) Apoptosis results of flow cytometry in each group. Full-length blots/gels are presented in Supplementary Fig. 5. The samples were derived from the same experiment and processed in parallel. ACTA2, actin alpha 2; ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMSCs, bone mesenchymal stem cells; CASP3, caspase 3; COL1A1, collagen type I alpha 1 chain; IL, interleukin; JAK, Janus-activated kinase; LT, liver transplantation; STAT, signal transducer and activator of transcription; TBil, total bilirubin. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001