Study on the Protective Effects of Schisandrin A on Hepatic Fibrosis Induced by Carbon Tetrachloride in Mice and Its Mechanism
- VernacularTitle:五味子甲素对四氯化碳诱导小鼠肝纤维化的保护作用及其机制研究
- Author:
Xiaohui WANG
1
;
Lin ZHOU
2
,
3
;
Qiuzheng DU
2
,
3
;
Yingying SHI
2
,
3
;
Ziwei JING
2
,
3
;
Liwei LIU
2
,
3
;
Jun ZHANG
2
,
3
;
Zhuolun LI
2
,
3
;
Xuedong JIA
2
,
3
;
Yaojuan CHU
2
,
3
;
Zhi SUN
2
,
3
;
Lihua ZUO
2
,
3
;
Jian KANG
2
,
3
;
Xiaojian ZHANG
2
Author Information
1. Dept. of Ultrasonography，the First Affiliated Hospital of Zhengzhou University，Zhengzhou 450052，China
2. Dept. of Pharmacy，the First Affiliated Hospital of Zhengzhou University，Zhengzhou 450052，China
3. Henan Precision Medicin e Clinical Mass Spectrometry Engineering Research Center，Zhengzhou 450052，China
- Publication Type:Journal Article
- Keywords:
Liver fibrosis;
Schisandrin A;
NLRP3/NF-κB signaling pathway;
TGF-β/Smad signaling pathway;
Mice
- From:
China Pharmacy
2020;31(22):2725-2730
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE：To study the pr otective effect of schisandrin A （SA）on CCl 4-induced liver fibrosis model mice and its mechanism. METHODS ：Mice were randomly divided into blank control group ，model group ，silymarin group （positive control，100 mg/kg），SA low-dose and high-dose groups （20，40 mg/kg），with 10 mice in each group. Except for blank control group，other groups were given CCl 4 subcutaneously to induce liver fibrosis model. After successful modeling ，administration groups were given relevant medicine intragastrically ，once a day ，for consecutive 6 weeks；blank control group and model group were given constant volume of 0.5％sodium carboxymethyl cellulose solution intragastrically by the same way. HE staining was used to observe the pathological changes of liver tissue in mice. UV spectrophotometry and ELISA assay were adopted to detect the serum levels of liver injury indexes （ALT and AST ）and the contents of inflammatory factors （TNF-α，IL-1β，IL-6）. Western blotting assay was used to detect the expression of NOD like receptor protein 3（NLRP3）/NF-κB and TGF-β/Smad signaling pathway protein. RESULTS ：Compared with blank control group ，obvious pathological changes of liver fibrosis were observed in model group. The serum levels of liver injury indexes and contents of inflammatory factors were significantly increased （P＜0.01）. The expression of NLRP 3，apoptosis associated spot-like protein ，Caspase-1 and IL- 1β，TGF-β1 and ratios ofp-NF-κB p65/NF-κB p65，p-IκBα/IκBα，p-Samd3/Smad3 were increased significantly （P＜0.01）. Compared with model group ，SA could significantly relieve hepatic fibrosis in mice ，reduce serum levels of liver injury indexes and contents of inflammatory factors ，as well as the expression of NLRP 3/NF-κB and TGF-β/Smad signaling pathway protein and phosphorylation level（P＜0.01）. CONCLUSIONS ： SA can effectively relieve liver injury and inflammation of CCl 4-induced hepatic fibrosis model mice ，which may be through the regulation of NLRP 3/NF-κB and TGF-β/Smad3 signaling pathways ，thus inhibiting the process of liver fibrosis.
