摘要
目的:探讨葛根素对兔肺缺血再灌注后肺组织Bcl-2、Bax、caspase-3蛋白表达的影响及意义。方法:健康日本大耳白兔30只,随机分为对照组(C组)、肺缺血再灌注组(IR组)及葛根素组(Pur组),复制单侧肺缺血再灌注损伤模型。对比观察各组血清超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量、肺湿干重比(W/D)、肺泡损伤数(IQA)及肺组织细胞凋亡指数(AI),免疫组化技术检测肺组织Bcl-2、Bax和caspase-3蛋白的表达。结果:与C组比,IR组的SOD活力降低(P<0.01),而MDA、W/D、IQA、AI值及Bcl-2、Bax、caspase-3蛋白表达均上调(均P<0.01)。Pur组与IR组相比,MDA、W/D、IQA、AI值及Bax、caspase-3蛋白表达明显下降(P<0.05或P<0.01);SOD、Bcl-2蛋白及Bcl-2/Bax则显著升高(均P<0.01)。结论:葛根素可上调肺组织Bcl-2蛋白,下调Bax和caspase-3蛋白表达,从而抑制肺再灌注后肺组织细胞的异常凋亡,减轻肺缺血再灌注损伤。
Objective：To investigate the effect of puerarin on Bcl-2,Bax and caspase-3 in lung tissues of rabbits after lung ischemia-reperfusion and its significance. Methods： Rabbits used for unilateral lung ischemia-reperfusion model were randomly divided into 3 groups：Control group （C group）, ischemia-reperfusion group （IR group） and puerarin group（ Put group）. The activity of serum superoxide dismutase （SOD）, the content of serum malondialdehyde （MDA）, the wet to dry weight ratio of lung tissue （W/D） and the index of quantitative assessment of histologic lung injury （IQA） were measured respectively in different groups. At the sane time, apeptosis index（AI） and Bcl-2,Bax,caspase-3 protein expression were studied using TUNEL and immunocytochemistry techniques in the groups mentioned above. Results： The activity of SOD was significantly lower in IR group than that in C group （P〈0.01）; while the content of MDA, the value of W/D, IQA and AI,together with the expression of Bcl-2,Bax and caspase-3 protein were evidently higher （P〈0.01 respectively）. Pur group, in comparison with IR group, showed decreases of MDA, W/D, IOA,AI and expression of Bax, caspase-3 protein （P〈0.05 or P〈0.01）, while increase of SOD,Bcl-2 protein and Bcl-2/Bax ratio （P〈0.01 respectively）. Conclusion： Puerarin can produce a marked effect in restraining apoptosis induced by ischemia-reperfusion which aggravates lung induryby down-regulating Bcl-2 expression and up-regulating of Bax and Caspase-3 expression.
出处
《温州医学院学报》
CAS
2007年第2期126-129,共4页
Journal of Wenzhou Medical College
基金
温州市科技局科研基金资助项目(Y2005A80)。
