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作 者:寇俊杰[1] 贾魁[1] 赵继义[1] 王际鹏[1] 柯雪莲[1] 李树云[1] 赵英玲 张跃东
机构地区:[1]哈尔滨医科大学第一附属医院心内四科,150001 [2]黑龙江省监狱管理局中心医院
出 处:《中华临床医师杂志(电子版)》2012年第16期4737-4740,共4页Chinese Journal of Clinicians(Electronic Edition)
基 金:黑龙江省自然科学基金(D201055)
摘 要:目的探讨无创性肢体缺血预适应对心肌梗死后心肌细胞凋亡及HSP70表达的影响。方法将健康成年雄性Wistar大鼠48只,随机平均分成4组:对照组(C),缺血再灌注组(I/R),经典缺血预适应组(IP),远程缺血预适应组(NDLIP)。各组分别在心肌梗死,再灌注过程中记录心电,再于实验末测定血清肌酸激酶(CK),肌酸激酶同工酶(CKMB),最后取心脏以免疫组化法检测热休克蛋白70(HSP70),以TUNEL法检测心肌细胞凋亡率,行心脏缺血范围(AAR)和梗死范围测定(IA),并计算梗死范围与缺血范围(IA/AAR)的比值。结果 (1)CK和CKMB:远程预适应组同经典预适应组的血清CK和CKMB值与缺血再灌注组相比明显下降(P<0.05);(2)心肌梗死面积(坏死区占缺血范围心肌重量的百分比):远程预适应组同经典预适应组的心肌梗死面积与缺血再灌注组相比明显下降(P<0.05);(3)凋亡率:远程预适应组同经典预适应组的凋亡率与缺血再灌注组相比明显下降(P<0.05);(4)HSP70:远程预适应组同经典预适应组的HSP70表达与缺血再灌注组相比表达增强(P<0.05)。结论远程缺血预适应同经典缺血预适应一样对大鼠心肌具有保护作用,其保护机制可能部分通过上调热休克蛋白以降低心肌细胞凋亡实现。Objective To investigate the effect of non-invasive limb ischemic preconditioning on myocardium apoptosis and HSP70 expression.Methods Male healthy adult Wistar rats weighing 200-300 g were used for this study.The rats were randomly assigned to four groups:control(A),ischemia/reperfusion(B),classic ischemic preconditioning(C),and remote ischemic preconditioning(D).Electrocardiogram were recorded during myocardial infarction and reperfusion.At the end of reperfusion,serum creatine kinase(CK),CK-MB,apoptosis index of myocardial cells with the methods of TUNEL,the expression of HSP70 using immunohistochemistry,area of the heart ischemia(area at risk AAR),the scope of infarction(infracted area,IA)and IA/AAR ratio were determined.Results (1)CK and CK-MB:The level of CK and CK-MB of C,D group were lower than B group(P<0.05).(2)Myocardial infarction area(IA/AAR):Myocardial infarction area(IA/AAR)of C,D group were lower than B group(P<0.05).(3)Apoptosis index:the apoptosis index of C,D group were lower than B group(P<0.05).(4)HSP70:The expression of HSP70 of C,D group were higher than B group(P<0.05).Conclusions We conclude that non-invasive limb ischemic preconditioning,as well as classic ischemic preconditioning,have cardioprotective effect which may be partly induced by increasing the level of HSP70 to inhibit apoptosis of myocardium.
关 键 词:再灌注损伤 HSP70热休克蛋白质类 细胞凋亡 远程缺血预适应
分 类 号:R542.22[医药卫生—心血管疾病]
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