The expression of AT1 receptor on hepatic stellate cells in rat fibrosis induced by CCl4
10.3760/j.issn:0366-6999.2001.06.005
- VernacularTitle:表达AT1受体对肝星状细胞功能调控: RAS抑制剂抗肝纤维化的实验研究
- Author:
Hongshan WEI
1
;
Hanming LU
;
Dingguo LI
;
Yutao ZHAN
;
Zhirong WANG
;
Xin HUANG
Author Information
1. Xinhua Hospital Shanghai Second Medical University
- Keywords:
hepatic fibrosis;
enalapril;
losartan;
renin-angiotensin system;
receptor
- From:
Chinese Medical Journal
2001;114(6):583-587
- CountryChina
- Language:Chinese
-
Abstract:
Objectives To assess the effect of an ACE inhibitor and an Ang Ⅱ type 1 (AT1) receptor antagonist on preventing hepatic fibrosis induced by CCl4 in rats and to investigate whether there is the expression of AT1 receptors on hepatic stellate cells. Methods Studies were conducted in male Sprague-Dawley rats. Except for model group and control group, in three treated groups, either enalapril (5?mg/kg), or losartan (10?mg/kg), or enalapril+losartan were given to the fibrotic rats (daily gavage). Saline vehicle was given to the control group. After 6 weeks, liver fibrosis was assessed directly by hepatic morphometric analysis. The expression of AT1 receptors and α-smooth muscle actin (α-SMA) in liver tissue and isolated hepatic stellate cells (HSC) were detected by immunohistochemical techniques. Results Compared with the fibrosis in rats of the model group, rats treated with either enalapril or losartan, or a combination of two drugs, showed a limited expansion of the interstitium (P<0.05), but no significant difference was observed among the three treated groups (P>0.05). The expression of AT1 receptors was found in abundance in the fibrotic interstitium of the fibrotic rats, whereas in the normal control rats they were limited to the vascular wall. AT1 receptors were also expressed on activated HSC in culture plates. Conclusions Angiotensin-converting enzyme inhibitors and AT1 blockers might slow the progression of hepatic fibrosis. Activated HSCs expressed AT1 receptors. Activation of RAS might be related to hepatic fibrogenesis induced by CCl4.
