Mechanism of hepatic stellate cell proliferation and apoptosis in rats by promoting circulation, removing stasis, and dredging collaterals based on the theory of liver collateral disease

Abstract

This study aims to investigate the impacts on the proliferation, inhibition, apoptosis, and cell cycle of hepatic stellate cells (HSC-T6) in rats by using traditional Chinese medicine (TCM) in serum. Twenty-seven rats were randomly divided into nine groups on average: a blank control (BC) group (fed by distilled water), a positive control group (colchicine solution, 0.05 mg/mL), and seven TCM groups [with the aim of clearing the liver of choleresis with 0.24 g/mL (weight of TCM herbs per milliliter), 0.73 g/mL, 1.22 g/mL, 2.45 g/mL, 7.34 g/mL, 12.24 g/mL, 24.48 g/mL]. Each rat received gavage with a dose of 1 mL/100 g twice a day for 7 days to prepare the drug serum. The HSC-T6 were divided into a TCM serum group, a positive control group, and a BC group. The TCM group and the positive control group were given corresponding drug serum for incubation, while the BC group received the medium without drug serum. The cellular proliferation inhibition rate in the positive control and TCM groups was significantly higher (P<0.01) than that in the BC group. The number of cells in the positive, 0.24 g/mL TCM, 1.22 g/mL TCM, and 7.34 g/mL TCM groups increased significantly (P<0.05) in the G0/G1 phase compared with the BC group. The number of cells in the positive group and all the TCM groups clearly increased in phase S by 0.73 g/mL in the TCM group, 2.45 g/mL in the TCM group, 12.24 g/mL in the TCM group, and 24.48 g/mL in the TCM group compared with the BC group, and the difference was statistically significant (P<0.05). The number of cells in the G2/M phase of the positive control group and all the TCM groups decreased significantly. Compared with the BC group, the positive group, 0.24 g/mL TCM group, 0.73 g/mL TCM group, 1.22 g/mL TCM group, 2.45 g/mL TCM group have statistically difference (P<0.05). A Qinggan Lidan prescription may exert anti-hepatic fibrosis effects by blocking HSC-T6 in the G0/G1 and S phases and by suppressing the proliferation of HSC-T6.