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目的探讨缺血后处理对大鼠离体心脏缺血再灌注损伤的作用及相关机制。方法 36只Wistar大鼠(257-326g),随机分为3组,对照组(Con组),缺血再灌注组(IR组),缺血后处理组(IPo C组)。采用Langendorff灌流装置建立缺血再灌注损伤模型,TTC染色评价梗死面积,Western blot检测凋亡蛋白及内质网应激相关通路蛋白表达。结果 IR组较Con组梗死面积增加,而Bcl-2表达显著降低,GRP78、CHOP、cleaved caspase12、cleaved caspase3、Bax及p-PERK表达水平显著增加。缺血后处理显著缩小梗死面积,并部分逆转相关蛋白表达的变化。结论缺血后处理减轻大鼠离体心脏缺血再灌注损伤,可能与抑制PERK通路介导的ERS相关凋亡相关。
Objective To investigate the effect and mechanism of ischemic postconditioning on ischemia-reperfusion injury in isolated rat hearts. Methods Thirty - six Wistar rats (257-326g) were randomly divided into three groups: control group (Con group), ischemia - reperfusion group (IR group) and ischemic postconditioning group (IPo C group). The ischemia-reperfusion injury model was established by Langendorff perfusion apparatus. The area of infarction was evaluated by TTC staining. Western blot was used to detect the expression of apoptosis-related proteins and endoplasmic reticulum stress-related pathways. Results Compared with Con group, the infarct size increased and the expression of Bcl-2 significantly decreased in IR group. The expression of GRP78, cleaved caspase12, cleaved caspase3, Bax and p-PERK were significantly increased. Ischemic postconditioning significantly reduced the infarct size and partially reversed the changes in the protein expression. Conclusion Ischemic postconditioning attenuates ischemia-reperfusion injury in isolated rat heart in vitro and may be related to the inhibition of PERK pathway-mediated ERS-related apoptosis.