Fig. 8.

RIPK3 knockdown in HSCs impairs the effect of curcumol on attenuating hepatic fibrosis. (A, B) Mice were randomly divided into the following 5 groups (eight mice every group): vehicle control, CCl₄, CCl₄ + curcumol 15 mg kg⁻¹, CCl₄ + curcumol 30 mg kg⁻¹ and CCl₄ + curcumol 60 mg kg⁻¹. The expression of RIPK1, RIPK3 in liver sections were detected by immunofluorescence staining. Scale bar, 100 µm. Mice were randomly divided into 5 groups (eight mice every group): vehicle control (no CCl₄, no treatment); CCl₄ + NC shRNA lentivirus; CCl₄ + curcumol + NC shRNA lentivirus; CCl₄ + RIPK3 shRNA lentivirus; and CCl₄ + RIPK3 shRNA lentivirus + curcumol. (C) Representative photograph of liver tissues, and microphotograph of H&E-stained, Masson-stained and Sirius Red-stained paraffin-embedded sections of liver tissues. Scale bar, 100 µm. (D) Immunochemical staining for α-SMA of liver sections. Scale bar, 100 µm. (E, F) Western blot analyses of RIPK1, p-RIPK1, RIPK3, p-RIPK3, α-SMA, and α1(I)-procollagen protein levels in isolated HSCs. Data are expressed as mean ± SD (n = 6); *P < 0.05 versus CCl₄, **P < 0.01 versus CCl₄, and ***P < 0.001 versus CCl₄, ^##P < 0.01, ^###P < 0.001 versus vehicle control. ^& P < 0.05 versus curcumol, ^&& P < 0.01 versus curcumol.