摘要
目的观察促红细胞生成素(EPO)对大鼠再灌注心律失常的影响,并对其机制进行初步探讨。方法以左冠状动脉前降支(LAD)穿线结扎法制备心肌缺血模型,松开结扎线造成再灌注。45只SD大鼠随机分成5组:①假手术(SHAM)组、②缺血再灌注(IR)组、③磷脂酰肌醇-3-激酶(PI3K)的高选择性阻断剂LY294002(LY)组、④促红细胞生成素(EPO)组和⑤促红细胞生成素+LY294002(EPO+LY)组。观察各组大鼠在整个缺血再灌注期间心律失常发生情况,进行室性心律失常评分;检测血清肌酸磷酸激酶同功酶MB(CK-MB)和肌钙蛋白I(cTnI)水平;以硫代巴比妥酸显色法测定心肌组织丙二醛(MDA)的含量;以黄嘌呤氧化酶法测定心肌组织超氧化物歧化酶(SOD)的含量。结果EPO组的心律失常评分明显低于IR、LY和EPO+LY组,差异有统计学意义(P<0.05);EPO血清CK-MB和cTnI水平组明显低于于IR、LY和EPO+LY组(P<0.001);EPO组SOD含量明显高于IR、LY和EPO+LY组,差异有统计学意义(P<0.001);EPO组MDA含量明显低于IR、LY和EPO+LY组,差异有统计学意义(P<0.001)。结论EPO 1000mg/kg再灌注前给药能有效降低大鼠再灌注心律失常的发生率,但此作用可被预先给予的LY294002所减弱,其作用机制与抗氧化作用有关,PI3K/Akt通路参与其信号转导。
Objective To explore the effect of erythropoietin （EPO） on reperfusion arrhythmias in rats and identify the possible mechanism involved, Methods Forty-five SD rats were randomized into a sham-operated group and 4 cardiac ischemia/reperfusion （IR） injury groups, which were further divided into IR group, LY294002 group, EPO group, and EPO＋LY294002 group. Cardiac IR injury was induced in the 4 IR injury groups by ligating the left anterior descending branch of the coronary artery （LAD） for 30 min followed by repefusion for 3 h, with subsequent treatments accordingly. The occurrence of arrhythrnias was monitored and scored during experiment, and the levels of serum CK-MB and cTnI were detected. The content of MDA in the myocardium was determined by thiobarbituric acid （TBA） method, and the content of SOD by xanthine oxidase method. Results The arrhythmia score in EPO group was significantly lower than those in IR, LY294002 and EPO＋ LY294002 groups （P〈0.05）. The levels of serum CK-MB and cTnI were significantly lower in EPO group than in the other 3 IR groups （P〈0.001）. The EPO group showed also significantly lower MDA content （P〈0.001） and higher SOD content than the other 3 IR groups （P〈0.001）. Conclusion EPO at the dose of 1000 mg/kg decreases the incidence of reperfusion arrhythmias in rats, and this effect can be attenuated by LY294002 pretreatrnent, suggesting that the cardioprotective effect of EPO involves antioxidation mediated by the phosphoinositide 3-kinase （PI3K） pathway.
出处
《南方医科大学学报》
CAS
CSCD
北大核心
2009年第6期1219-1222,共4页
Journal of Southern Medical University
