Abstract

To explore the inhibition of artesunate on liver fibrosis and to clear its mechanism of inhibiting anti-liver fibrosis by blocking epithelial-mesenchymal transition and regulating c-Jun N-terminal kinase pathway. Randomly take 18 male Sprague–Dawley rats. Set 6 untreated rats from them as control groups. Construct a rat model of liver fibrosis with another 12 rats and give intraperitoneal injection of a 50 % carbon tetrachloride olive oil solution for 1 ml/kg. After successful modeling, randomly divide them into model group and artesunate group, with 6 rats in each group. The artesunate group received 20 mg.kg^-1.d^-1 intragastric gavage and the rest 2 groups were given equal amounts of normal saline. Compare and analyze the function indexes of rat’s livers (i.e. alanine aminotransferase and aspartate aminotransferase). Quantificational and in real time, detect the messenger ribonucleic acid expression of alpha-smooth muscle actin and collagen I in liver tissues by polymerase chain reaction and the expression of alpha-smooth muscle actin, collagen I, Slug, N-cadherin and c-Jun N-terminal kinase-related pathway protein by Western blot. The alanine aminotransferase and aspartate aminotransferase concentration of rat’s serum in the artesunate group were obviously lower than that in the model group and the difference was of statistical significance (p<0.05). The messenger ribonucleic acid expression of alpha-smooth muscle actin, collagen I and protein content in the artesunate group were dramatically lower compared with the model group and the difference was of statistical significance (p<0.05). Masson staining tests showed that there was no obvious liver tissue fiber deposition in the control group and liver tissue was normal in morphology, while in the model group, a large amount of collagen fiber deposition was discovered in liver tissue. And the area of liver tissue collagen fibers obviously shrunk in the artesunate group compared with the model group. The content of Slug and N-cadherin in the hepatic tissue of artesunate group was much lower than that in the model group and the difference was of statistical significance (p<0.05). The protein content of p-c-Jun N-terminal kinase and p-c-Jun in hepatic tissue of the artesunate group was much lower than that in the model group and the difference was statistically significant (p<0.05). Artesunate can effectively inhibit the progress of liver fibrosis and the mechanism may have something to do with blocking the epithelial–mesenchymal transition and regulating the c-Jun N-terminal kinase pathway.