Pirfenidone inhibits TGF-β/Smad signaling pathway to alleviate hepatic cirrhosis induced by carbon tetrachloride
10.3969/j.issn.1000-484X.2019.02.007
- VernacularTitle:吡菲尼酮抑制TGF-β/Smad信号通路缓解四氯化碳诱导的小鼠肝硬化
- Author:
Xue FENG
1
;
Yi LI
;
Tan-Sheng CHEN
;
Yong-Qin YU
;
Qi-Jun LÜ
Author Information
1. 胜利油田中心医院感染科
- Keywords:
Pirfenidone;
TGF-β/Smad signaling pathway;
Liver cirrhosis;
Carbon tetrachloride
- From:
Chinese Journal of Immunology
2019;35(2):161-164
- CountryChina
- Language:Chinese
-
Abstract:
Objective: This research aimed to explore the therapeutic effect and its mechanism of pirfenidone in liver cirrhosis induced by carbon tetrachloride in mice. Methods: Sixty male C57 BL/6 mice were randomly divided into the control group, model group and different doses of pirfenidone group, twelve rats in each group. Mice were intraperitoneally injected with 20％ CCl4 soybean oil solution ( 5 ml/kg), twice a week for 7 weeks. And these mice were free to drink 20％ ethanol solution in the third week after building the model. The low, medium and high dose groups were respectively given 50, 100 and 200 mg/kg of pirfenidone solution according to the body weights, while the model group and control group were given equal volume of blank solvent after building the model, once a day for 2 weeks. The serum level of ALT and AST, liver index, spleen index, the gene or protein expression level of TGF-β1 and Smad3 were analyzed before and after the treatment of pirfenidone. Results: The serum level of ALT, AST increased significantly in the model group ( P＜0. 05), while decreased significantly in different doses of pirfenidone group ( P＜0. 05). The liver and spleen index in the model group was significantly higher than that in the control group ( P＜0. 05). However, after treating with pirfenidone, the liver and spleen index were significantly lower than that in the model group ( P＜0. 05). The number of TGF-β1 positive cells in the model group was significantly more than that in the control group, but it was significantly decreased in the pirfenidone group. The gene expression level of Smad3 in the model group was significantly higher than that in the control group ( P＜0. 05). The gene expression level of TGF-β1 and Smad3 in different doses of pirfenidone group were significantly lower than that in the model group ( P＜ 0. 05). Meanwhile, the protein level of TGF-β1 and Smad3 were significantly increased in the model group, while decreased in the pirfenidone group. Conclusion: Pirfenidone relieves liver cirrhosis caused by carbon tetrachloride in mice by inhibiting the TGF-β1/Smad3 signaling pathway.
