Effects of ATP sensitive potassium channel opener on the mRNA and protein expressions of caspase-12 after cerebral ischemia-reperfusion in rats
- VernacularTitle:ATP敏感性钾通道开放剂对大鼠脑缺血再灌注后caspase-12 mRNA及蛋白表达的影响
- Author:
ZHANG HONG
1
;
SONG LI-CHUN
;
JIA CHUN-HONG
;
LU YONG-LI
Author Information
1. 中国医科大学附属盛京医院
- Keywords:
ATP sensitive potassium channel;
cerebral ischemia;
apoptosis;
endoplasmic reticulum;
caspase-12
- From:
Neuroscience Bulletin
2008;24(1):7-12
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate effects of KATP 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 KATP 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, KATP opener group, and KATP 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 immunohistochemical staining, respectively. Results In ischemia-reperfusion group, KATP opener group and KATP 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 KATP opener group, The number of apoptotic cells was significantly less than that in ischemia-reperfusion group and KATP 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 KATP blocker group at all times (P ＜ 0.05 or P ＜ 0.01). There were no differences between the ischemia-reperfusion group and KATP blocker group at each time (P ＞ 0.05). Conclusion KATP opener may protect neurons from apoptosis following the cerebral ischemia-reperfusion by inhibiting ER stress pathway.
