机构地区:[1]Department of Neurology, the Affiliated Shengjing Hospital of China Medical University, Shenyang 110004, China [2]Department of Anatomy, China Medical University, Shenyang 110001, China
出 处:《Neuroscience Bulletin》2008年第1期7-12,共6页神经科学通报(英文版)
摘 要:Objective To investigate effects of K_ATP opener on the expressions of caspase-12 mRNA and protein, and to explore the role of endoplasmic reticulum (ER) stress pathway in the mechanism of K_ATP opener protecting against neuronal apoptosis after cerebral ischemia-reperfusion. Methods Two hundred rats were randomly divided into four groups: sham operation group, ischemia-reperfusion group, K_ATP opener group, and K_ATP blocker group. The middle cerebral artery occlusion (MCAO) model was established by intraluminal suture occlusion method; neuronal apoptosis was detected by TUNEL staining. The mRNA and protein expressions of caspase-12 were detected by semi-quantitative RT-PCR and immunohisto-chemical staining, respectively. Results In ischemia-reperfusion group, K_ATP opener group and K_ATP blocker group, the number of apoptotic cells and the mRNA and protein expressions of caspase-12 gradually increased following cerebral reperfusion, and reached the peak at 24 h. In K_ATP opener group, The number of apoptotic cells was significantly less than that in ischemia-reperfusion group and K_ATP blocker group at 12 h, 24 h, 48 h and 72 h (P 〈 0.05 or P 〈 0.01); while the mRNA and protein levels of caspase-12 were significantly less than those in ischemia-reperfusion group and K_ATP blocker group at all times (P 〈 0.05 or P〈0.01). There were no differences between the ischemia-reperfusion group and K_ATP blocker group at each time (P〉 0.05). Conclusion K_ATP opener may protect neurons from apoptosis following the cerebral ischemia-reperfusion by inhibiting ER stress pathway.Objective To investigate effects of K_ATP opener on the expressions of caspase-12 mRNA and protein, and to explore the role of endoplasmic reticulum (ER) stress pathway in the mechanism of K_ATP opener protecting against neuronal apoptosis after cerebral ischemia-reperfusion. Methods Two hundred rats were randomly divided into four groups: sham operation group, ischemia-reperfusion group, K_ATP opener group, and K_ATP blocker group. The middle cerebral artery occlusion (MCAO) model was established by intraluminal suture occlusion method; neuronal apoptosis was detected by TUNEL staining. The mRNA and protein expressions of caspase-12 were detected by semi-quantitative RT-PCR and immunohisto-chemical staining, respectively. Results In ischemia-reperfusion group, K_ATP opener group and K_ATP blocker group, the number of apoptotic cells and the mRNA and protein expressions of caspase-12 gradually increased following cerebral reperfusion, and reached the peak at 24 h. In K_ATP opener group, The number of apoptotic cells was significantly less than that in ischemia-reperfusion group and K_ATP blocker group at 12 h, 24 h, 48 h and 72 h (P 〈 0.05 or P 〈 0.01); while the mRNA and protein levels of caspase-12 were significantly less than those in ischemia-reperfusion group and K_ATP blocker group at all times (P 〈 0.05 or P〈0.01). There were no differences between the ischemia-reperfusion group and K_ATP blocker group at each time (P〉 0.05). Conclusion K_ATP opener may protect neurons from apoptosis following the cerebral ischemia-reperfusion by inhibiting ER stress pathway.
关 键 词:ATP sensitive potassium channel cerebral ischemia APOPTOSIS endoplasmic reticulum CASPASE-12
分 类 号:R322.81[医药卫生—人体解剖和组织胚胎学]
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