不同预处理后缺血再灌注损伤大鼠心肌αB晶状体蛋白的变化
Change of myocardial alpha B-crystallin after different kinds of preconditioning against ischemia/reperfusion injury in rats
摘要目的 研究3种不同预处理对在体大鼠缺血再灌注心肌的保护作用及αB晶状体蛋白在不同预处理心肌细胞缺血再灌注损伤中的变化.方法 24只SD大鼠按完全随机法分成4组,每组6只,分别为缺血再灌注组、缺血预处理组、腺苷预处理组、远程预处理组.建立大鼠在体缺血再灌注损伤模型,观察各组缺血再灌注前后心功能变化,并检测冉灌注末血清肌钙蛋白T(cTnT)、丙二醛(MDA)、超氧化物歧化酶(SOD)的变化以及心肌组织αB品状体蛋白的表达.结果 心肌缺血再灌注120 min后,与缺血再灌注组比较,其余3组左心室室内压最大上升和下降速率(±dp/dt_(max))均明显升高(均P<0.05).缺血预处理组、腺苷预处理组、远程预处理组血清cTnT含量均低于缺血再灌注组[(12.898±2.887)、(5.049±4.387)、(7.049±4.387)μg/L比(22.902±3.146)μg/L,均P<0.05];MDA含量也均低于缺血再灌注组[(10.648±3.635)、(11.736±8.903)、(9.834±6.128)μmol/L比(16.083±10.423)μmol/L,均P<0.05];SOD含量均高于缺血再灌注组[(82.808±22.407)、(162.266±54.128)、(102.266±34.134)U/ml比(76.757±39.446)U/ml,均P<0.05].腺苷预处理组SOD含量高于缺血预处理组和远程预处理组;cTnT含量则低于缺血预处理组(均P<0.05).与缺血再灌注组比较,其余3组αB晶状体蛋白表达均显著增高(均P<0.05).结论 腺苷预处理、远程预处理均可以模拟缺血预处理的心肌保护作用.3种预处理可能通过上调αB晶状体蛋白表达从而减轻在体大鼠心肌缺血再灌注损伤.
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abstractsObjective To evaluate the cardioprotective effects of three different preconditioning methods and the change of myocardial α B-crystallin after these preconditioning methods against ischemia /reperfusion injury in rats. Methods Twenty-four SD rats were randomly divided into 4 groups (n=6 each): ischemia reperfusion group (IR), ischemia preconditioning group (IP), adenosine preconditioning group (AP) and remote preconditioning group (RP). The ischemia/reperfusion rat models were established in vivo. Hemodynamics of heart function before and after ischemia/reperfusion was recorded. At the end of reperfusion, serum cardiac troponin T (cTnT), malondialdehyde (MDA) , superoxide dismutase (SOD) and expression of α B-crystallin in myocardium were detected. Results At 120 minutes after reperfusion, significant increase in ±dp/dt_(max), was recorded in rats of group IP, AP and RP as compared with those of group IR (all P<0.05). Lower level of serum cTnT [(12.898±2.887), (5.049±4.387), (7.049±4.387) μg/L vs (22.902±3.146) μg/L, all P<0.05] was found in group IP, AP and RP as compared to group IR, so was the level of MDA [ (10.648±3.635), (11.736±8.903), (9.834±6.128) μmol/L vs (16.083±10.423) μmol/L,all P<0.05] ; but the level of SOD was just the reverse [(82.808±22.407), (162.266±54.128), (102.266± 34.134) U/ml vs (76.757±39.446) U/ml, all P<0.05]. Expression of αB-crystallin in these three groups was significantly higher than that in IR group (all P<0.05). AP group had a higher SOD level compared with IP and RP groups and a lower level of cTnT compared with IP group (all P<0.05). Conclusion Remote preconditioning and adenosine preconditioning may mimic the protective effects of ischemic preconditioning. Preconditioning attenuates myocardial isehemia/reperfusion injury in vivo possibly through up-regulation of αB-crystallin expression in rats.
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