【摘要】 探讨信号分子p38MAPK在心肌缺血再灌注损伤中的作用。SD雄性大鼠分为4组,即:N组(伪手术组),A组(缺血再灌注组),B组(缺血再灌注+黄芪干预组),C组(缺血再灌注+硝酸甘油干预组)。其中根据不同缺血时间各组又分为2亚组:A1、B1、C1组为缺血30 min再灌注;A2、B2、C2组为缺血60 min再灌注。术前/中监测心电图变化,模型成功72 h后观察左室压变化,随后取血检测心肌酶谱变化,取心肌组织检测p38MAPK的表达。A1组、A2组的血清心肌酶含量值(CK、CKMB、LDH、AST)均高于对照组(N组),左室压变化值均低于对照组;相同缺血时间段比较,B、C组的各心肌酶含量值低于A组,B、C组左室压变化值低于对照组,而高于A组,差异均极显著(P<0.01)。A1组、A2组的p38MAPK含量高于对照组,B1、C1组高于A1组,差异均极显著(P<0.01);B2、C2组高于A2组,差异显著(P<0.05)。心肌缺血再灌注可激活p38MAPK信号途径,从而减轻心肌再灌注损伤。更多还原

【Abstract】 The role of the signaling factor p38MAPK was studied on myocardial Ischemia-reperfusion injury based on the animal models. SD male rats were divided into four groups randomly( group N: sham group,group A1: ischemic 30 min and reperfusion, group A2: ischemic 60min and reperfusion,group B1: ischemic 30 min-reperfusion and Astragalus Membranaceus treatment,group B2: ischemic 60min and Astragalus Membranaceus treatment,group C1: ischemic 30min and Nitroglycerin treatment,group C2: ischemic 60 min and Nitroglycerin). The changing of ECG in preparation and operation was inspected. After 72 of the operation,the levels of myocardial zymogram were determined and the left ventricular pressure was traced. After that,the expression about p38MAPK was observed by tocking myocardium. Myocardium zymogram( include CK、CKMB、LDH and AST) in the group A1、A2were significantly higher than that of group N respectively. In the same ischemia times,these value in the group B、C were obviously lower than that of group A( P < 0. 01). While the reverse phenomenon were obtained about left ventricular pressure. The expression about p38MAPK in the group A1、A2were significantly higher than that of group N respectively,and group B1、C1were also significantly higher than group A1( P <0. 01). This value in the group B2、C2was only higher than that of group A2( P <0. 05). Myocardial Ischemia-Reperfusion can activate p38MAPK signaling transduction path,then reduce Ischemia-reperfusion injury.更多还原