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大黄素对肝纤维化大鼠肺损伤的保护作用
引用本文:张丽丽,张慧英,王黎敏,李旭炯,贾建桃,吕敏丽,范毅敏,张翠英,刘明社,赵中夫,韩德五,CHENGJi.大黄素对肝纤维化大鼠肺损伤的保护作用[J].中国病理生理杂志,2014,30(2):291-296.
作者姓名:张丽丽  张慧英  王黎敏  李旭炯  贾建桃  吕敏丽  范毅敏  张翠英  刘明社  赵中夫  韩德五  CHENGJi
作者单位:长治医学院 1病理生理学教研室, 2机能实验室, 3生理学教研室, 5肝病研究所,山西 长治 046000; 山西医科大学 4第二医院ICU,6肝病研究所,山西 太原 030001; 7南加州大学Keck医学院肝病研究中心,美国 加利福尼亚州 洛杉矶 90089
基金项目:国家自然科学基金(No.81070339);山西省国际科技合作计划(No.2010081068);山西医科大学细胞生理学省部共建教育部重点实验室主任基金资助项目(No.2010-09);山西省回国留学人员科研基金资助项目(No.211-091)
摘    要: 目的:探讨不同剂量大黄素对肝纤维化大鼠肺损伤的保护作用。方法:采用复合致病因素法(CCl 4、乙醇、高脂、高胆固醇和低胆碱)建立肝纤维化大鼠模型并以不同剂量(20 mg/kg和40 mg/kg)大黄素进行治疗。4周后,测定肝指数,检测血清内毒素、同型半胱氨酸、反映肝功能的指标白蛋白、天门冬氨酸氨基转移酶、丙氨酸氨基转移酶、总胆红素、总胆固醇、甘油三酯和肝纤维化指标透明质酸、层黏连蛋白、Ⅳ型胶原蛋白、Ⅲ型前胶原蛋白的含量,观察肝组织病理学改变; 测定肺指数,光镜下行肺组织病理学观察,检测肺组织匀浆肿瘤坏死因子α(TNF-α)、丙二醛(MDA)、一氧化氮(NO)和过氧亚硝基阴离子(ONOO-)含量。结果:大鼠肝纤维化模型复制成功,模型组大鼠肺指数明显增加,肺脏发生水肿、炎症反应,肺匀浆TNF-α、MDA、NO和ONOO-含量明显增加;大黄素治疗组肺指数较模型组下降,肺组织病理性损伤明显减轻,肺组织TNF-α、MDA、NO和ONOO-含量明显降低。结论:大黄素对肝纤维化大鼠的肺损伤具有一定的保护作用。

关 键 词:大黄素  肝纤维化  肝肺综合征  肺损伤  
收稿时间:2013-09-17

Protective effect of emodin on lung injury induced by hepatic fibrosis in rats
ZHANG Li-li,ZHANG Hui-ying,WANG Li-min,LI Xu-jiong,JIA Jian-tao,L Min-li,FAN Yi-min,ZHAN Cui-ying,LIU Ming-she,ZHAO Zhong-fu,HAN De-wu,CHENG Ji.Protective effect of emodin on lung injury induced by hepatic fibrosis in rats[J].Chinese Journal of Pathophysiology,2014,30(2):291-296.
Authors:ZHANG Li-li  ZHANG Hui-ying  WANG Li-min  LI Xu-jiong  JIA Jian-tao  L Min-li  FAN Yi-min  ZHAN Cui-ying  LIU Ming-she  ZHAO Zhong-fu  HAN De-wu  CHENG Ji
Affiliation:1Department of Pathophysiology, 2Functional Integrative Laboratory, 3Department of Physiology, 5Institute of Hepatology, Changzhi Medical College, Changzhi 046000, China; 4ICU of The Second Hospital, 6Institute of Hepatology, Shanxi Medical University, Taiyuan 030001, China; 7Research Center for Liver Disease, Keck School of Medicine, University of Southern California, Los Angeles, CA 90089, USA.
Abstract:AIM:To explore the protective effect of emodin on lung injury induced by hepatic fibrosis in rats. METHODS:The hepatic fibrosis rat model was established with multiple pathogenic factors (CCl 4, ethanol, high fat, high cholesterol and low choline) and treated with different doses (20 mg/kg and 40 mg/kg) of emodin for 4 weeks. The hepatic index was measured. The biochemical indexes, endotoxin, homocysteine, albumin, aspartate aminotransferase,alanine aminotransferase, total bilirubin, total cholesterol and triglyceride, and hepatic fibrosis indexes, hyaluronic acid, laminin, collagen IV and procollagen Ⅲ, were detected. The histopathological changes of the liver were observed. The pulmonary index was determined. The histopathological changes of the lungs were observed. The levels of tumor necrosis factor α (TNF-α), malondialdehyde (MDA), nitric oxide (NO) and peroxynitrite (ONOO-) in the lung tissues were analyzed. RESULTS:The rat hepatic fibrosis model was successfully established. In model group, lung edema and inflammation occurred, and the pulmonary index and the levels of TNF-α, MDA, NO and ONOO- in the lung tissues were increased significantly. In emodin treatment groups, the pulmonary indexes were lower than that in model group. The pathological injury of the lung tissues was alleviated. The levels of TNF-α, MDA, NO and ONOO- in the lung tissues were decreased. CONCLUSION:Emodin has a protective effect on lung injury induced by hepatic fibrosis in rats.
Keywords:Emodin  Liver fibrosis  Hepatopulmonary syndrome  Lung injury
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