| 黄芩苷对D-氨基半乳糖致大鼠急性肝衰竭的保护作用 |
| 投稿时间：2011-05-23 修订日期：2011-05-30 点此下载全文 |
| 引用本文：申春燕,陈永平,阳韬,陆小蒟,李春艳.黄芩苷对D-氨基半乳糖致大鼠急性肝衰竭的保护作用[J].医学研究杂志,2012,41(2):87-91 |
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| 中文摘要:目的观察黄芩苷对大鼠急性肝衰竭的保护作用并探讨可能机制。方法86只大鼠随机分为正常对照组、模型组和黄芩苷组，模型组和黄芩苷组再分为1、3、5、7天4个亚组。采用腹腔注射D-氨基半乳糖建立大鼠急性肝衰竭动物模型，黄芩苷组于造模后每隔12h腹腔注射黄芩苷（120mg/kg）1次。全自动生化仪检测血清ALT、AST和TBil水平； HE染色观察肝组织病理学变化；RT-PCR法检测肝组织Bax、Bcl-2、caspase-3 mRNA表达；蛋白免疫印迹法检测肝组织Bax、Bcl-2蛋白表达量。统计学处理采用方差分析。结果黄芩苷组肝组织损伤程度明显轻于模型组。黄芩苷组大鼠各时间点血清ALT、AST、TBil水平较模型组明显降低（t=18.85,15.63,8.86；P均<0.01）。黄芩苷组肝组织Bax、Bcl-2、caspase-3 mRNA的表达趋势与模型组一致，随时间延长3天时达高峰，5、7天时逐渐降低，与模型组相比Bax、caspase-3 mRNA表达量明显降低（t=-55.51,-16.20；P均<0.01）、Bcl-2 mRNA表达量较模型组升高（t=51.91，P<0.01）。黄芩苷组Bax、Bcl-2蛋白表达趋势与模型组一致，Bax蛋白表达量较模型组明显降低（t=-21.32，P<0.01），Bcl-2蛋白表达量较模型组明显升高（t=50.91，P<001）；黄芩苷组各时间点Bcl-2/Bax蛋白比率明显高于模型组（t=68.08,58.11,64.04,17.50；P均<0.01）。结论黄芩苷可以通过上调抗凋亡基因Bcl-2的表达和下调促凋亡基因Bax，进而减少caspase-3的表达，保护D-GalN诱导的大鼠急性肝衰竭。 |
| 中文关键词:黄芩苷 急性肝衰竭 Bax Bcl-2 半胱天冬酶-3 |
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| Protective Effect of Baicalin on Acute Liver Failure in Rats |
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| Abstract:ObjectiveTo study the protective effect of baicalin against acute liver failour in rats and to explor its mechanism.MethodsEighty-six male SD rats were randomly divided into normal group,model group and baicalin group. The model group and baicalin group were respectively divided into 4 subgroups:1,3,5,7days.The animal model of acute liver failour was established by intraperitoneal injection with D-galactosamine(D-GalN). Baicalin (120mg/kg) was treated intraperitoneally (ip) at every 12h after D-GalN injected in rats.The levels of ALT，AST and TBil in serum were detected with automatic biochemical analyzer. Sections of liver tissue were stained with hematoxylin-eosin and were observed under optical microscope．Semiquantitive PCR was used to study the expression of Bax，Bcl-2 and caspase-3 mRNA in the lives. Western blotting used to study the expression of Bax and Bcl-2 protein.ResultsCompared with model group,the liver tissues damage of baicalin group was significantly reduced.Compared with model group, the levels of ALT,AST and TBil of baicalin group were significantly reduced. The discrepancy between model group and baicalin group had statistical significance（t=18.85,15.63,8.86；P<0.01）. Compared with modele group,the tendency of Bax,Bcl-2 and caspase-3 mRNA expression in baicalin group was in accordance with the model group,which reached a peak at 3d with the time extending and later gradually reduced,and the discrepancy between model group and baicalin group had statistical significance(P<0.05). The expressions of Bax and caspase-3 mRNA in baicalin group were significantly reduced at different time point comapred with the model group（t=-55.51,-1620；P<001）, while the expressions of Bcl-2 mRNA were significantly increased at different time point comapred with the model group（t=5191,P<0.01）. The tendency of Bax and Bcl-2 protein expression in baicalin group was in accordance with the model group. The expressions of Bax protein were significantly reduced at different time point comapred with the model group（t=-21.32,P<0.01）, but the expressions of Bcl-2 protein were significantly increased at different time point comapred with the model group（t=5091,P<0.01）.The rate of Bcl-2 to Bax of baicalin group at different time points was greater than the model group （t=68.08,5811,64.04,17.50；P<001）.ConclusionBaicalin can protect rats against acute liver failure by down-regulating Bax expression and up-regulating Bcl-2 expression in liver tissue and reducing of pro-inflammatory cytokines. |
| keywords:Baicalin Acute liver failour Bax Bcl-2 Caspase-3 |
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