黄芩茎叶总黄酮对缺氧/复氧诱导的心肌细胞凋亡相关基因Bcl-2、Bax表达的影响

目的:探讨黄芩茎叶总黄酮(scutellaria baicalelensis stem leaf total flavonoid SSTF)对培养的乳鼠心肌细胞缺氧/复氧时凋亡相关基因Bcl-2、Bax蛋白表达的影响。方法:原代培养乳鼠心肌细胞,缺氧(hypoxia H)2h后,复氧(reoxygenation R)4h制备缺氧/复氧损伤模型。以免疫组织化学方法检测心肌细胞Bcl-2、Bax蛋白表达变化。心肌细胞损伤程度以心肌细胞存活率表示。结果:缺氧2h再复氧4h,心肌细胞Bcl-2蛋白阳性表达指数(positive expressionindex PEI)显著低于对照组(P<0.01),Bax蛋白PEI显著高于对照组(P<0.01)。细胞存活率明显低于对照组(P<0.05)。SSTF干预组Bcl-2蛋白PEI明显高于缺氧/复氧组(P<0.05),Bax蛋白PEI显著低于缺氧/复氧组(P<0.05),细胞存活率明显高于缺氧/复氧组(P<0.05)。结论:心肌细胞缺氧再复氧时,Bcl-2蛋白表达降低,Bax蛋白表达增强;细胞存活率降低。SSTF可通过上调Bcl-2蛋白表达,抑制Bax蛋白表达,减少细胞凋亡,从而减轻心肌细胞缺氧/复氧损伤。

Effects of SSTF on the protein Expression of Apoptosis-associated Bcl-2 and Bax Genes in Cultured Neonatal Rat Cardiomyocytes with Hypoxia/reoxygenation

Objective: To study the effects of SSTF on the protein expression of apoptosis-associated Bcl-2Bax genes in cultured neonatal rat cardiomyocytes with hypoxia/reoxygenation.Methods: Neonatal rat cardiomyocytes in primary culture were exposed to hypoxia for 2 hours and subsequently reoxygenation for 4 hours.The change of protein expressions of Bcl-2 and Bax genes were detected by immunohistochemistry respectively.Colorimetric assay was used to detect cell viability to evaluate the degree of cardiomyocyte injury.Results: Compared with that of the sham operation group,the positive expression index (PEI) of Bcl-2 protein in cardiomyocytes was decreased significantly (P<0.01) and the PEI of Bax protein in cardiomyocytes was increased significantly (P<0.01) after 2 hours of hypoxia and 4 hours of reoxygenation.Cell viability was decreased obviously after hypoxia/reoxygenation (P<0.05).Compared with that of the hypoxia/reoxygenation group,in the SSTF group the PEI of Bcl-2 protein was increased significantly (P<0.05) and the PEI of Bax protein was decreased significantly (P<0.05),and the cell viability was increased obviously (P<0.05).Conclusion: In cultured neonatal rat cardiomyocytes,the protein expression of Bcl-2 gene decreases and the protein expression of Bax gene increases during hypoxia/reoxygenation.Cell viability decreases during hypoxia/reoxygenation.SSTF can protect myocardium against hypoxia/reoxygenation injury by up-regulating Bcl-2protein expression and by inhibiting Bax protein expression.