作为促分裂原活化蛋白激酶（mitogen-activaled protein kinase，MAPK）超家族成员之一的c-Jun氨基末端激酶（c-Jun N-terminal kinase，JNK）家族是与细胞增殖、分化或凋亡调控密切相关的细胞内信号转导通路。目前越来越多的报道证实了...作为促分裂原活化蛋白激酶（mitogen-activaled protein kinase，MAPK）超家族成员之一的c-Jun氨基末端激酶（c-Jun N-terminal kinase，JNK）家族是与细胞增殖、分化或凋亡调控密切相关的细胞内信号转导通路。目前越来越多的报道证实了JNK信号途径具有促凋亡和抗凋亡的双重功能，这种双重功能受到细胞类型、刺激物的种类、剂量和持续时间以及胞内其他信号途径的影响。此综述主要探讨JNK在心肌缺血／再灌注（ischemic／reperfusion，I／R）损伤，缺血预处理（ischemic preconditioning，IPC）和缺血后处理中涉入机制及调节作用。展开更多
目的探讨缺血后处理对大鼠局灶性脑缺血/再灌注损伤的保护作用及与内质网应激通路相关分子GRP78、caspase-12的关系。方法成年雄性Wistar大鼠58只,随机分为假手术组(sham组)、缺血/再灌注组(I/R组)和缺血后处理组(IP组),采用线栓法阻断...目的探讨缺血后处理对大鼠局灶性脑缺血/再灌注损伤的保护作用及与内质网应激通路相关分子GRP78、caspase-12的关系。方法成年雄性Wistar大鼠58只,随机分为假手术组(sham组)、缺血/再灌注组(I/R组)和缺血后处理组(IP组),采用线栓法阻断大脑中动脉制备大鼠局灶性脑缺血/再灌注(MCAO)模型。大鼠脑缺血/再灌注后24 h进行神经行为学评分和脑梗死体积测定;脑缺血/再灌注6 h、12 h、24 h后免疫组织化学方法检测脑缺血侧半暗带区GRP78、caspase-12蛋白的表达。结果与缺血/再灌注组相比,后处理组再灌注24h神经行为学评分明显降低,脑梗死体积明显减少(P<0.05);后处理组再灌注12 h、24 h GRP78蛋白表达明显增加,再灌注24 h caspase-12蛋白表达明显减少。结论脑缺血后处理可能通过减弱内质网应激过程从而对随后发生的再灌注损伤起到了神经保护作用。其机制可能是增加GRP78蛋白表达、减少caspase-12蛋白表达而减轻神经细胞的凋亡。展开更多
The phenomenon of ischemia/reperfusion injury is described in the experimental models of acute myocardial infarction（AMI）,causing additional functional and structural damage to the acute reperfused myocardium,and is...The phenomenon of ischemia/reperfusion injury is described in the experimental models of acute myocardial infarction（AMI）,causing additional functional and structural damage to the acute reperfused myocardium,and ischemic preconditioning refers to the myocardial ischemia after a long period of reperfusion before one or several shortoccasional duplication of myocardial ischemia /reperfusion1,which can increase myocardial ischemic tolerance.The therapeutic strategies for AMI have focused on myocardial ischemia /reperfusion injury,which accounts for a significant part of the final infarct size.Although experiments in the last 20 years have reported that pharmacological interventions at reperfusion might reduce myocardial reperfusion injury,this could not be confirmed in human studies.An alternative to chemical modifiers,postconditioning（brief repeated periods of ischemia applied at the onset of reperfusion） is another method proven to be efficient in animal models and to be confirmed in recent human studies.This simple method,applied in the first minute of reperfusion,reduces the final infarct size by 30%-50%.This review will focus on the mechanisms,pharmacological preconditioning,postconditioning technique,which is easily applicable in human patients in the setting of AMI.展开更多
文摘目的探讨缺血后处理对大鼠局灶性脑缺血/再灌注损伤的保护作用及与内质网应激通路相关分子GRP78、caspase-12的关系。方法成年雄性Wistar大鼠58只,随机分为假手术组(sham组)、缺血/再灌注组(I/R组)和缺血后处理组(IP组),采用线栓法阻断大脑中动脉制备大鼠局灶性脑缺血/再灌注(MCAO)模型。大鼠脑缺血/再灌注后24 h进行神经行为学评分和脑梗死体积测定;脑缺血/再灌注6 h、12 h、24 h后免疫组织化学方法检测脑缺血侧半暗带区GRP78、caspase-12蛋白的表达。结果与缺血/再灌注组相比,后处理组再灌注24h神经行为学评分明显降低,脑梗死体积明显减少(P<0.05);后处理组再灌注12 h、24 h GRP78蛋白表达明显增加,再灌注24 h caspase-12蛋白表达明显减少。结论脑缺血后处理可能通过减弱内质网应激过程从而对随后发生的再灌注损伤起到了神经保护作用。其机制可能是增加GRP78蛋白表达、减少caspase-12蛋白表达而减轻神经细胞的凋亡。
文摘The phenomenon of ischemia/reperfusion injury is described in the experimental models of acute myocardial infarction（AMI）,causing additional functional and structural damage to the acute reperfused myocardium,and ischemic preconditioning refers to the myocardial ischemia after a long period of reperfusion before one or several shortoccasional duplication of myocardial ischemia /reperfusion1,which can increase myocardial ischemic tolerance.The therapeutic strategies for AMI have focused on myocardial ischemia /reperfusion injury,which accounts for a significant part of the final infarct size.Although experiments in the last 20 years have reported that pharmacological interventions at reperfusion might reduce myocardial reperfusion injury,this could not be confirmed in human studies.An alternative to chemical modifiers,postconditioning（brief repeated periods of ischemia applied at the onset of reperfusion） is another method proven to be efficient in animal models and to be confirmed in recent human studies.This simple method,applied in the first minute of reperfusion,reduces the final infarct size by 30%-50%.This review will focus on the mechanisms,pharmacological preconditioning,postconditioning technique,which is easily applicable in human patients in the setting of AMI.
