黄芩苷对大鼠心肌缺血再灌注时细胞凋亡的影响

目的:研究黄芩苷对大鼠心肌缺血再灌注时细胞凋亡的影响。方法:结扎大鼠左冠状动脉前降支复制心肌缺血再灌注损伤模型,黄芩苷100mg/kg于冠脉结扎前10min静脉注射后,再灌注结束后称重法检测心肌梗死面积,分光光度法测定组织丙二醛(MDA)含量和超氧化物歧化酶(SOD)和髓过氧化物酶(MPO)活性,原位末端标记(TUNEL)法和HE染色观察凋亡心肌细胞和组织病理学改变。结果:黄芩苷可明显抑制缺血再灌注所致心肌梗死面积增大,降低组织MDA、MPO含量,升高SOD活性,抑制心肌细胞凋亡和炎性细胞浸润。结论:黄芩苷可通过抑制心肌细胞凋亡而保护缺血再灌注心肌。

Effects of baicalin on apoptosis induced by myocardial ischemia reperfusion in rats

Aim: To study the effects of baicalin on apoptosis of myocardium induced by ischemia reperfusion in rats. Method: The myocardial ischemia/reperfusion injury model in rats was established by left anterior descending coronary occlusion, followed by reperfusion for 240 min. Baicalin 100mg/kg was injected intravenously 10min before occlusion. The area of myocardial infarction, content of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and myeloperoxidase (MPO) in tissue were measured by weighing or spectrometry, respectively. The apoptosis and pathological change of myocardium was detected by TUNEL and HE staining. Result: Baicalin reduced the area of cardial infarction and the content of MDA and MPO induced, elevated the SOD activiy in heart, inhibited apoptosis of myocardium, and neutrophil infiltration induced by ischemia-reperfusion. Conclusion: Baicalin has a protective effect on myocardial ischemia/ reperfuion injury through inhibiting myocardium apoptosis.