Beta-sitosterol alleviates liver fibrosis in mice by blocking tprl-smad2/3 and TNF-a-nf-icb signaling pathways
10.3969/j.issn.1001-1978.2020.01.016
- Author:
Xing WAN
1
Author Information
1. Medical College, Dept of Functional Sciences
- Publication Type:Journal Article
- Keywords:
Beta-sitosterol;
Liver fibrosis;
Nuclear factor kb;
Smad2/3;
Tgfp receptor 1;
Tnp-a
- From:
Chinese Pharmacological Bulletin
2020;36(1):75-80
- CountryChina
- Language:Chinese
-
Abstract:
Aim To explore the effect of beta-sitosterol (BS) on liver fibrosis induced by CCL4 in mice and the mechanisms. Methods Fifty C57BL/6 male mice were randomly divided into five groups; control group (CG) , carbon tetrachloride group (CTG), low/medium/high dose of BS group ( BS-L/M/H), with 10 mice in each group. The model of hepatic fibrosis was established by injecting CCL4 in peritoneal cavity, the study lasted 30 days, and different doses of BS were given from 1st day to 15 th day. All mice were sacrificed for the observation of morphological changes and the measurement of liver index. Liver collagenous fibers were observed by HE and Masson staining, the changes of serum ( ALT and AST) were assessed by Elisa, the expressions of a-SMA and Collagen I were detected by Western blot and immunohistochemistry, and the changes of TpRl-Smad2/3 and TNF-a-NF∗kB were detected by Elisa and Western blot. Results Compared to control group, different doses of BS markedly inhibited the increase of liver index, A .T, AST, a-SMA and Collagen I in a dose-dependent n an-ner ( P < 0. 05 or P < 0. 01 ). Liver morphology, inflammatory cell infiltration and collagenous fiber irj BS groups were better than those in CCL4 group, meanwhile BS-M decreased the expression of TgKl, Smad2/3, TNF-a and p-NF-KB (P <0. 01). Conclusions BS dose-dependently inhibits mouse liver f bro-sis induced by CCL4, and its mechanism may be related to inhibiting TpRl-Smad2/3 and TNF-a-N •-kB signaling pathways.
