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目的观察ATP敏感性钾通道(KATP)开放剂对大鼠脑缺血再灌注后caspase-12mRNA和蛋白表达的影响,探讨内质网信号通路是否参与了KATP开放剂对脑缺血后神经元凋亡的抑制机制。方法200只Wistar雄性大鼠随机分为假手术组,缺血再灌注组,开放剂组及阻断剂组。应用线栓法制备大鼠大脑中动脉缺血再灌注模型,分别应用免疫组化染色、RT-PCR技术检测脑缺血再灌注后各组caspase-12蛋白及mRNA的表达。结果在缺血再灌注组,开放剂组及阻断剂组,随着缺血再灌注时间的延长,caspase-12mRNA及蛋白的表达逐渐增高,在缺血再灌注后24h达高峰。开放剂组caspase-12mRNA及蛋白表达在各时间点均显著少于缺血再灌注组及阻断剂组(P<0.05或P<0.01)。阻断剂组各时间点与缺血再灌注组相比均无显著性差异(P>0.05)。结论KATP开放剂可能通过抑制内质网信号通路,减少神经元凋亡,降低脑缺血再灌注损伤。
Objective To investigate the effect of ATP-sensitive potassium channel (KATP) opener on the expression of caspase-12 mRNA and protein after cerebral ischemia-reperfusion in rats and to explore whether endoplasmic reticulum signaling pathway is involved in the neuronal apoptosis after cerebral ischemia Inhibition of death mechanism. Methods 200 Wistar male rats were randomly divided into sham operation group, ischemia reperfusion group, opener group and blocker group. The middle cerebral artery occlusion (MCAO) model of rat middle cerebral artery occlusion (MCAO) was prepared by thread occlusion method. The expressions of caspase-12 protein and mRNA in each group were detected by immunohistochemical staining and RT-PCR respectively. Results The expression of caspase-12 mRNA and protein increased gradually with the time of ischemia-reperfusion in ischemia-reperfusion group, opener group and blocker group, reaching the peak at 24h after ischemia-reperfusion. The expression of caspase-12 mRNA and protein in opener group was significantly less than those in ischemia-reperfusion group and blocker group at all time points (P <0.05 or P <0.01). There was no significant difference in the blocking agent group compared with the ischemia-reperfusion group at each time point (P> 0.05). Conclusion KATP opener may reduce neuronal apoptosis and decrease cerebral ischemia-reperfusion injury by inhibiting the endoplasmic reticulum signaling pathway.