远程预处理对心肌缺血-再灌注损伤的保护作用  

Protection of remote ischemic preconditioning on myocardial ischemia-reperfusion injury

作　　者：钟敏[1] 肖建斌[1] 周娜[1] 招伟贤[1] 

机构地区：[1]广东省中医院麻醉科,广州市510120

出　　处：《临床麻醉学杂志》2011年第11期1107-1109,共3页Journal of Clinical Anesthesiology

基　　金：广东省医学科研基金资助项目(A2008244)

摘　　要：目的观察远程预处理对急性心肌缺血-再灌注损伤的保护作用及对心肌信号转导和转录活化因子3(STAT3)蛋白的影响。方法健康雄性Wistar大鼠48只,体重240～280g,随机均分为三组:对照组(N组)、缺血-再灌注组(IR组)、远程预处理组(rIPC组)。N组仅穿线不结扎血管;IR组结扎左冠状动脉前降支(LAD)30min,再灌注120min;rIPC组在LAD结扎前以止血带捆绑双下肢阻断血流5min,放松5min,反复4次。实验结束后用TTC染色法测定大鼠心肌梗死面积;取下腔静脉血3ml离心后测定血中磷酸肌酸酶(CK)及乳酸脱氢酶(LDH)含量;WesternBlot法测定总STAT3(t-STAT3)和磷酸化STAT3(p-STAT3)蛋白表达水平。结果 rIPC组心肌梗死面积较IR组明显缩小(P<0.05),N组无心肌梗死;IR组CK及LDH含量较N组显著升高(P<0.01),rIPC组CK及LDH含量较IR组明显降低(P<0.01);三组之间t-STAT3表达差异无统计学意义,IR组p-STAT3表达较N组显著降低(P<0.05),rIPC组p-STAT3表达较IR组明显升高(P<0.05)。结论远程预处理对心脏缺血-再灌注损伤具有早期保护作用,其机制可能与增加心肌p-STAT3蛋白表达有关。Objective To investigate the role of the signal transducer and activator of transcription 3 （STAT3） in the cardiaoprotection of remote ischemic preconditioning. Methods The rat model of cardiac ischemic-reperfusion injury was generated by occluding left anterior descending artery（LAD） for 30 min followed by reperfusion for 120 min. Forty-eight male Wistar rats weighing 240-280 g were divided into three groups randomly： group N,sham-surgery control group; group IR, ischemia-reperfusion group; group rIPC, four cycles of 5 min of both hind limbs ligation before LAD occlusion. The area of infarct size, the serum levels of creatine phosphokinase （CK） and lactose dehydrogenase（LDH） were measured. The protein expressions of both total and phosphorylated STAT3 were determined by Western boltting. Results Compared with group IR, the myocardial infarct size in group rIPC was significantly smaller（P〈0.05）. The serum levels of CK and LDH significantly increased in group IR compared with group N（P〈0.01）, while decreased in group rlPC compared with group IR（P〈0.01）. The expression of total STAT3 was not different significantly among three groups. Expression of phosphorylated STAT3 was higher in group rIPC than that in group IR（P〈0.05）, while lower in group IR than that in group N（P〈0.05）. Conclusion This results suggest that remote ischemiac preconditioning may be able to protect the heart against reperfusion injury mediated by increasing the phosphorylation of STAT3.

关 键 词：远程预处理 心肌缺血-再灌注损伤 信号转导和转录活化因子3 

分 类 号：R542.2[医药卫生—心血管疾病]