摘要
目的:研究壮肝逐瘀煎对肝纤维化(HF)大鼠TβRⅠ/Ⅱ、Smad3、Smad4和Smad7表达的影响.方法:Wistar大鼠44只,随机取8只作为正常对照(A)组;余大鼠用CCl4复合因素法进行HF造模,wk4随机处死4只证实HF形成后随机分为病理模型(B)组、壮肝逐瘀煎治疗(C)组、秋水仙碱对照(D)组、大黄蟅虫丸对照(E)组.B组予生理盐水ig,C、D、E组予相应药液ig.6wk后获取肝组织,HE染色观察HF程度;用免疫组化、图像分析方法对TβRⅠ/Ⅱ、Smad3、Smad4、Smad7的组织分布进行半定量分析.结果:与B组比较,C、D、E组肝小叶结构趋于正常,肝组织TβRⅠ/Ⅱ、Smad3、Smad4表达显著减少(TβRⅠ:2.75±0.10,3.14±0.07,3.44±0.06vs5.47±0.13,P<0.01;TβRⅡ:1.86±0.12,2.09±0.10,2.53±0.12vs3.52±0.15,P<0.01;Smad3:2.28±0.59,3.84±1.11,3.97±0.90vs5.65±1.28,P<0.01;Smad4:1.57±0.53,3.15±0.79,3.37±0.78vs5.25±1.60,P<0.01),Smad7表达显著增加(3.45±0.58,2.09±0.38,1.75±0.29vs0.73±0.34,P<0.01),C组强于D、E组(P<0.01).结论:壮肝逐瘀煎能显著改善HF组织病理变化,其作用机制可能与壮肝逐瘀煎调控TβRⅠ/Ⅱ、Smad3、Smad4、Smad7的表达有关.
AIM: To investigate the effects of Zhuanggan Zhuyu Decoction (ZZD) on the expression of TβRⅠ/Ⅱ, Smad3, Smad4 and Smad7 in experimental liver fibrosis of rats, and to explore its anti-fibrotic molecular mechanism.
METHODS: Forty-four Wistar rats were used inthis study, 8 of which were selected as normal controls (group A), and the rest were used to establish liver fibrosis model with carbon tetrachloride (CC1,) and combined factors. At the 4th wk, four rats were executed to confirm the formation of liver fibrosis, and then the rest of rats were randomly divided into the pathological model group (B), ZZD-treated group (C), colchicine-treated group (D) and Dahuang Zhechong Pill-treated group (E). The rats in group B were treated (ig) with saline. At the end of the 6th wk, the formation of hepatic fibrosis was observed by HE staining and the expression of TβRⅠ/Ⅱ, Smad3, Smad4 and Smad7 were detected by SP immunohistochemistry.
RESULTS: Six weeks later, in comparison with that in group B, the structure of liver lobules almost restored to normal in groups C, D and E; the fibrous septum became thinner; the expression of TβRⅠ/Ⅱ, Smad3 and Smad4 were also significantly decreased (TβRⅠ 2.75 ± 0.10, 3.14 ± 0.07, 3.44 ± 0.06 vs 5.47 ± 0.13, P 〈 0.01; TβRⅡ 1.86 ± 0.12, 2.09 ± 0.10, 2.53 ± 0.12 vs 3.52 ± 0.15, P 〈 0.01; Smad3:2.28 ± 0.59, 3.84 ± 1.11, 3.97 ± 0.90 vs 5.65 ± 1.28, P 〈 0.01; Smad4:1.57 ± 0.53, 3.15 ± 0.79, 3.37 ± 0.78 vs 5.25 ± 1.60, P 〈 0.01), whereas the expression of Smad7 was significantly increased (3.45 ± 0.58, 2.09 ± 0.38, 1.75 ± 0.29 vs 0.73 ± 0.34, P 〈 0.01). The effect in group C was stronger than that in group D or E, and the dif- ferences were significant (both P 〈 0.01). CONCLUSION: ZZD can reverse liver fibrosis induced by CC1, and combined factors and the mechanism may be associated with its effect on regulating and controlling the expression of TβRⅠ/Ⅱ, Smad3, Smad4 and Smad7.
出处
《世界华人消化杂志》
CAS
北大核心
2008年第10期1105-1109,共5页
World Chinese Journal of Digestology
基金
国家自然科学基金资助项目
No.30460158~~