The inhibitory effect of salvianolic acid B on Hepa1-6 cells and tumor-bearing mice

AimTo investigate the inhibitory effect of salvianolicacid B (Sal B) on mouse hepatocellular carcinoma cells (Hepa1-6) and to explore its role through the TGF-β1/Smad2 signaling pathway.MethodsHepa1-6 cells were divided into the control group, TGF-β1 stimulation group, and TGF-β1+Sal B group. Cell proliferation and migration ability were assessed. PSmad2C, pSmad2L expression levels, pSmad2C, pSmad2L and Smad2 protein changes were detected using cellular immunofluorescence. Tumorigenic mice were randomly divided into the model group, Sal B (7.5 mg·kg-1·d-1) group, Sal B(15 mg·kg-1·d-1) group, Sal B(30 mg·kg-1·d-1) group, and colchicine group(0.1 mg·kg-1·d-1), with 8 mice in each group. Body weight, tumor volume changes, tumor histopathology, pSmad2C, pSmad2L protein changes were all detected.ResultsSal B effectively inhibited the TGF-β1 induced proliferation and migration of Hepa1-6 cells, concomitantly reducing the protein expression levels of pSmad2C and pSmad2L. In vivo, Sal B potently suppressed tumor growth in a xenograft model in a dose-dependent manner. Histopathological (HE) staining and Western blot analysis further confirmed that Sal B treatment inhibited tumor growth and down-regulated the protein expression of pSmad2C and pSmad2L in tumor tissues.ConclusionsSal B exhibits a significant inhibitory effect on the growth of Hepa1-6 cells stimulated by TGF-β1, and this mechanism may be closely associated with the activation of the TGF-β1/Smad2 signaling pathway. Furthermore, the inhibitory effect of Sal B on TGF-β1-induced tumor growth in vivo is likely mediated through the activation of the TGF-β1/Smad2 signaling pathway.