RESUMO
OBJECTIVE: To observe the effect of chlorogenic acid on the secretion of inflammatory cytokines and regulation mechanism of P38MAPK, NF-κB signaling pathway in human hepatic stellate cells induced by TGF-β1. METHODS: Different concentrations of CGA worked in normal and activated hepatic stellate cells to make sure the appropriate drug concentration. The exponential growth phase cells were randomly divided into normal HSC group, normal HSC + CGA group, after cultured 48 h, the cells were cultured with 0, 50, 100 mg·L-1 CGA for 24 h; HSC( TGF-β1) group, HSC( TGF-β1 + CGA) group: after 24 h, the cells were induced by 10 μg·L-1 TGF-β1 for 24 h, and then cultured with 0, 50, 100 mg·L-1 CGA for 24 h. The expression of α-SMA protein was detected by immunocytochemistry, the expression of p-P38, P65 protein was detected by Westernblot, the expression of TNF-α, IL-6 mRNA was detected by real time quantitative PCR, and the content of TNF-α, IL-6 in the supernatant was detected by ELISA method. RESULTS: The appropriate concentrations of CGA were 50 and 100 mg·L-1, these concentration has no effect on normal HSC(P > 0.05); after stimulation by TGF-β1, the expression of α-SMA, p-P38, P65, TNF-α, IL-6 was increased(P < 0.01), when activated HSC cells were treated with 50 and 100 mg·L-1 CGA, the expression of α-SMA, p-P38, P65, TNF-α, IL-6 was decreased( P < 0.05, P < 0.01). CONCLUSION: CGA can inhibit the proliferation of activated HSC, regulate the secretion of inflammatory factors such as TNF-α, IL-6 by P38MAPK and NF-κB signaling pathway, inhibit the occurrence of liver fibrosis.