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作 者:章洁[1] 刘丽乔[1] 余乐涵[1] 赵小曼[1] 李华[1] 万福生[2]
机构地区:[1]南昌大学医学院生化与分子生物学教研室,南昌330006 [2]南昌大学实验动物科学部,南昌330006
出 处:《江西医学院学报》2007年第6期20-22,共3页Acta Academiae Medicinae Jiangxi
基 金:江西省自然科学基金资助项目(No0040054)
摘 要:目的观察川芎嗪对缺血再灌注损伤时心肌细胞凋亡的保护及初步机制。方法采用在体结扎大鼠冠状动脉左前降支建立心肌缺血再灌注模型。以TUNEL法检测心肌凋亡细胞,免疫组化法分析心肌细胞Fas/FasL、Caspase-8及Caspase-3蛋白表达变化。荧光分析法测定Caspase-3活性。结果凋亡组(心肌缺血1h,再灌注24h)心肌细胞凋亡指数为16.3±4.52,较对照组(0.43±0.04)有显著性升高,Fas/FasL及Caspase-3蛋白水平也均显著高于正常对照组(P<0.05)。川芎嗪保护组的心肌细胞凋亡指数、Fas/FasL、Caspase-3蛋白水平及Caspase-3活性均显著性低于凋亡组。结论川芎嗪对缺血再灌注损伤心肌细胞凋亡有较好的保护作用,其机制可能与降低Fas死亡受体通路中相关蛋白酶水平及其活性有关。Objective To investigate the protective effects of Liqustrazin on the apoptosis in rats with myocardial ischemia/reperfusion injury. Methods Rat modes with myocardial ischemia-reperfusion injury were established by occluding left coronary arter(LCA)and followed by release of it with ligation. Fifty rats were divided randomly into control group(sham operated for 24 h), apoptosis group(1 h of ischemia followed by 25 h of reperfusion), and Liqustrazin group(intraperitoneal injection of Liqustrazin 5 mg/kg, 10 mg/kg or 15 mg/kg respectively before ischemia fol- lowed by 24 h of reperfusion). Terminal deoxynucleotidy transferase-mediatde dUTP fluoescein nick end labeling(TUNEL)and S-P immunohistochemical staining were used respectively to determine the apoptosis and protein expression of Fas/FasL, Caspase-8 and Caspase-3 genes and its activity were detected by Fluorospectrophotometry. Results Apoptosis index, positive index of Fas/FasL and Caspase-8/3 protein expression were all increased in the rat's myocardium of apoptosis group,and the level of Caspase-3 activity increased. Liqustrazin was able to decrease signifi- cantly apoptosis index, positive index of Fas/FasL and Caspase-8/3 protein expression, and Caspase-3 activity in the ischemia-reperfusion myocardium. Conclusion Liqustrazin exerts a good antagonist action on the apoptosis of ischemia/reperfusion myocardial cells and signal transduction pathway of Fas death receptor.
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