OBJECTIVE: To study the therapeutic mechanism of salvianolic acid B (SA-B) in treating hepatic fibrosis. METHODS: Twenty-four Wistar rats were randomly divided into 3 groups: normal control group, untreated group and SA-B-treated group. Rats in the untreated and SA-B-treated groups were injected intraperitoneally with 0.5% dimethylnitrosamine (DMN) for 4 weeks, daily for 3 days each week at a dose of 10 microg/kg, to induce hepatic fibrosis. Then, rats in the SA-B-treated group were given SA-B orally for another 4 weeks. Hydroxyproline (Hyp) contents in liver tissue of the rats in 3 groups were determined with HCl hydrolysis, and collagen type I, transforming growth factor-beta 1 (TGF-beta1), transforming growth factor-beta receptor type I (TbetaRI) and transforming growth factor-beta receptor type II (TbetaRII) were detected by Western blotting. RESULTS: The Hyp content and the expressions of collagen type I, TGF-beta1, TbetaRI and TbetaRII in the liver tissue of rats in the untreated group increased significantly as compared with those in the normal control group, while those in SA-B-treated group decreased significantly as compared with those in the untreated group. CONCLUSION: The therapeutic mechanism of SA-B in treating hepatic fibrosis may be related to inhibiting the expressions of TGF-beta1 and its receptors.
OBJECTIVE: To study the therapeutic mechanism of salvianolic acid B (SA-B) in treating hepatic fibrosis. METHODS: Twenty-four Wistar rats were randomly divided into 3 groups: normal control group, untreated group and SA-B-treated group. Rats in the untreated and SA-B-treated groups were injected intraperitoneally with 0.5% dimethylnitrosamine (DMN) for 4 weeks, daily for 3 days each week at a dose of 10 microg/kg, to induce hepatic fibrosis. Then, rats in the SA-B-treated group were given SA-B orally for another 4 weeks. Hydroxyproline (Hyp) contents in liver tissue of the rats in 3 groups were determined with HCl hydrolysis, and collagen type I, transforming growth factor-beta 1 (TGF-beta1), transforming growth factor-beta receptor type I (TbetaRI) and transforming growth factor-beta receptor type II (TbetaRII) were detected by Western blotting. RESULTS: The Hyp content and the expressions of collagen type I, TGF-beta1, TbetaRI and TbetaRII in the liver tissue of rats in the untreated group increased significantly as compared with those in the normal control group, while those in SA-B-treated group decreased significantly as compared with those in the untreated group. CONCLUSION: The therapeutic mechanism of SA-B in treating hepatic fibrosis may be related to inhibiting the expressions of TGF-beta1 and its receptors.
Authors: Florent Duval; Jorge E Moreno-Cuevas; María Teresa González-Garza; Carlos Rodríguez-Montalvo; Delia Elva Cruz-Vega Journal: Chin Med Date: 2014-12-24 Impact factor: 5.455