The inhibitory effect of Euonymus alatus against mouse hepatic fibrosis induced by CCl4
10.3969/j.issn.1001-1978.2018.04.010
- VernacularTitle:鬼箭羽醇提物对四氯化碳诱导小鼠肝纤维化模型的作用
- Author:
Xing WAN
1
;
Qiong GUO
;
Xiang-Dong LIU
;
De-Bin HUANG
Author Information
1. 湖北民族学院医学院
- Keywords:
Euonymus alatus;
hepatic fibrosis;
ALT;
TNF-α;
α-SMA;
Collagen Ⅰ
- From:
Chinese Pharmacological Bulletin
2018;34(4):485-490
- CountryChina
- Language:Chinese
-
Abstract:
Aim To explore the inhibitory effect of Euonymus alatus on hepatic fibrosis induced by carbon tetrachloride (CCl4) in mice and its mechanism. Methods Eighty C57BL/6 male mice were randomly divided into eight groups: normal group, CCl4model group, Euonymus alatus(EA) ethanol extracts groups in early stage(EAE), EA ethanol extracts groups in later stage(EAL),two drug groups with low/medium/high dose(EAE-L/M/H, EAL-L/M/H), with 10 mice in each group. Fibrosis model was established by injecting CCl4in peritoneal cavity,and the study lasted for 30 days. Different doses of drugs were given from 1 st day to 15 th day in EAE while from 16 th day to 30 th day in EAL,then all mice were sacrificed to for the observation of the morphological changes and collage-nous fiber by HE and Masson staining. Liver index, ALT,AST and TNF-α were tested by ELISA. The ex-pressions of α-SMA and CollagenⅠwere measured by immunohistochemistry and Western blot. Results Compared to normal group, liver index, ALT, AST, TNF-α, α-SMA and CollagenⅠ in EA groups were lower than those in model group in a dose-dependent manner(P<0.01 or P<0.05). Liver morphology and collagenous fiber in EAE and EAL were better than those in model group in a dose-dependent manner. The effect of EAE were superior to that of the EAL in HE, Masson, α-SMA, Collagen Ⅰ indexes(P <0.05). Conclusions Euonymus alatus may inhibit the process of hepatic fibrosis in mice with dose-effect de-pendence, and drug treatment in early stage performs better,which may be related to the decrease of TNF-α that affects the expression of α-SMA and Collagen Ⅰ.
