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作 者:贾俊海[1] 陈素仙[2] 张志坚[3] 陈永昌[1]
机构地区:[1]江苏大学医学院生理学教研室,江苏镇江212001 [2]江苏大学医学院机能实验室,江苏镇江212001 [3]江苏大学医学院基础与临床医学研究中心,江苏镇江212001
出 处:《江苏大学学报(医学版)》2005年第5期384-386,共3页Journal of Jiangsu University:Medicine Edition
基 金:江苏大学青年自然科学基金(1241280002)
摘 要:目的:观察大鼠肾脏缺血预处理后心肌缺血再灌注时细胞间粘附分子-1(ICAM-1)表达的变化,探讨缺血预处理对心肌缺血再灌注损伤的影响。方法:大鼠30只,分为心肌缺血再灌注(M IR)组,M IR+肾脏缺血预处理(R IP)组和假手术对照(sham)组,取缺血心肌用原位杂交法检测ICAM-1 mRNA、免疫组织化学法检测ICAM-1蛋白质表达水平,观察分析心肌梗死范围、中性粒细胞计数等指标。结果:与Sham组比较,M IR组和M IR+R IP组各时相点ICAM-1 mRNA和蛋白质表达均显著增加。肾脏预处理后即刻ICAM-1mRNA和蛋白质表达与M IR组比较有所减少,但无统计学意义,R IP后24 h ICAM-1mRNA和蛋白质表达均显著减少(与M IR组比较,P<0.01)。结论:心肌缺血再灌注时,ICAM-1参与介导了中性粒细胞对组织细胞的粘附、浸润和心肌缺血再灌注的发生、发展,R IP可通过减少ICAM-1 mRNA及其蛋白质表达水平减轻M IR所致的心肌坏死。Objective: To observe the change of intercellular adhesion molecule expression in ischemicreperfused myocardium after renal ischemic preconditioning, and to investigate the effect of ischemic preconditioning on myocardial ischemic-reperfusion injure. Methods: Thirty rats were divided into three groups: MIR group, MIR + RIP group and Sham-group. The levels of expression of ICAM-1 mRNA in myocardia were evaluated by method of IN Situ Hybridization and the protein expression were evaluated by immunocytochemistry. The infarct sizes were measured and the numbers of PMNs were counted. Results: Compared with Sham-group, the expression levels of ICAM-1 mRNA and the protein in MIR and MIR + RIP groups were increased significantly. Compared with MIR groups, the expression levels of ICAM-1 mRNA and the protein were decreased significantly in 24 hours after RIP. Conclusion: The findings indicated that PMN could induce myocardial ischemic reperfusion injure after MIR, which resulted from the ICAM-1 mediated PMN adhesion. The results also suggested that RIP could decrease myocardial ischemic reperfusion injure induced by MIR and this action was mediated by the reduction of the expression of ICAM-1 mRNA and the protein.
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