[1]艾志波,张荣华,闫国和,等.鳖甲煎改良方对大鼠肝纤维化的作用及其机制研究[J].陆军军医大学学报(原第三军医大学学报),2011,33(03):274-277.
 Ai Zhibo,Zhang Ronghua,Yan Guohe,et al.Effect of modified turtle shell decoction on hepatic fibrosis in rats and its mechanism[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(03):274-277.
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鳖甲煎改良方对大鼠肝纤维化的作用及其机制研究(/HTML )
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陆军军医大学学报(原第三军医大学学报)[ISSN:1000-5404/CN:51-1095/R]

卷:
33卷
期数:
2011年第03期
页码:
274-277
栏目:
论著
出版日期:
2011-02-15

文章信息/Info

Title:
Effect of modified turtle shell decoction on hepatic fibrosis in rats and its mechanism
作者:
艾志波 张荣华闫国和粟永萍 艾国平
第三军医大学:西南医院中西医结合科;军事预防医学院全军复合伤研究所,创伤、烧伤与复合伤国家重点实验室
Author(s):
Ai Zhibo Zhang Ronghua Yan Guohe Su Yongping Ai Guoping
Department of Integrated Traditional Chinese and Western Medicine, Southwest Hospital, State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Combined Injury, College of Military Preventive Medicine, Third Military Medical University, Chongqing, 400038, China
关键词:
鳖甲煎改良方肝纤维化TGF-β1Smad3Smad7
Keywords:
modified turtle shell decoction hepatic fibrosis TGF-β1 smad3 smad7
分类号:
R285.5; R289.5; R575.05
文献标志码:
A
摘要:
目的   探讨鳖甲煎改良方对大鼠肝纤维化(hepatic fibrosis,HF)的作用及其机制。   方法     SD雄性大鼠90只,随机分6组,每组15只,其中以40%CCl4处理(3 ml/kg)8周复制中毒肝纤维化模型(模型组),复制模型的同时分别用鳖甲煎改良方高剂量组28.4 g/(kg·d)、中剂量组14.2 g/(kg·d)、低剂量组7.1 g/(kg·d) 灌胃治疗并且以复方鳖甲软肝片灌胃0.6 g/(kg·d)作阳性对照组治疗6周。以复制模型同样方式与用量于右后腿皮下注射橄榄油及生理盐水灌胃(10 ml/kg·d)作空白对照组。苏木精-伊红(HE)染色观察各组8周后肝纤维化变化程度,RT-PCR检测其转化生长因子β1(transforming growth factor beta one,TGF-β1)、Smad3及Smad7变化,免疫组化(S-P法)观测TGF-β1、smad3、smad7表达情况。   结果     8周后,与模型组比较,鳖甲煎改良方高、中、低剂量组和复方鳖甲软肝片组肝小叶结构破坏明显减轻,部分肝细胞脂肪变性,炎性细胞浸润与少量胶原纤维形成; 肝组织TGF-β1与Smad3的mRNA及蛋白表达显著减少(P<0.01),smad7 mRNA及蛋白表达明显增加(P<0.01)且鳖甲煎改良方高、中、低剂量组和复方鳖甲软肝片组疗效并无显著差异。   结论     鳖甲煎改良方能显著改善大鼠肝纤维化,其作用机制可能与鳖甲煎改良方调控TGF-β/smad信号通路有关。
Abstract:
Objective   To study the effect of modified turtle shell decoction (MPTSD) on hepatic fibrosis in rats and its mechanism.    Methods   Ninety male SD rats were randomly divided into 6 groups, 15 rats in each group. A toxic hepatic fibrosis of rats was reproduced with 40% carbon tetrachloride (CCl4) (3 ml/kg) for 8 weeks. Fifteen rats were treated for 6 weeks with MPTSD at 28.4 g/(kg·d) as a high dose group, at 14.2 g/(kg·d) as a medium dose group, and at 7.1 g/(kg·d) as a low-dose group. Rats treated with compound MPTSD soft tablets at 0.6 g/(kg·d) served as a positive control group and those treated with olive oil at 10 ml/(kg·d) served as a blank control group. Changes of HF in different groups were observed with hematoxylin-eosin(HE)staining 8 weeks after treatment. Expression of transforming growth factor beta 1 (TGF-β1), Smad3 and Smad7 was detected by reverse transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry staining.    Results   Eight weeks after treatment, the destruction of hepatic lobules in high, medium and low dose MPTSD groups and positive control group were remarkably alleviated with,fatty degeneration of some liver cells, infiltration of inflammatory cells and formation of few collagen fibers. The mRNA and protein expression level of TGF-β1 and Smad3 was significantly lower while the expression level of Smad7 was remarkably higher in high, medium and low dose MPTSD groups and positive control group than in blank control group(P<0.01) . No significant difference was observed in high, medium and low dose MPTSD groups and positive control group.    Conclusion   MPTSD can significantly improve CCl4- induced hepatic fibrosis in rats by regulating the TGF-β/smad signal pathway. 

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更新日期/Last Update: 2011-01-31