Neuronal apoptosis and expressions of Ire1α and caspase-12 in rats with spinal cord ischemia reperfusion injury
10.3760/cma.j.issn.1001-8050.2010.04.024
- VernacularTitle:大鼠脊髓缺血再灌注损伤中Ire1α、caspase-12的表达与细胞凋亡
- Author:
Jing LI
;
Shanquan SUN
;
Hui LIU
;
Xingye ZHANG
;
Baobing GAO
- Publication Type:Journal Article
- Keywords:
Reperfusion injury;
Endoplasmic reticulum;
Cell apoptosis;
Cysteine protein
- From:
Chinese Journal of Trauma
2010;26(4):349-353
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression changes of Ire1α and caspase-12 in rats with spinal cord ischemia-reperfusion injury.Methods Fifty-five adult SD rats(250-300 g)were randomly divided into control group(re=5)and operation group(n=50).The spinal cord ischemia-reperfusion models were established and the neuronal apoptosis was detected by terminal deoxynucleotidyl transferasemediated dUTP nick end labeling(TUNEL).The expressions of Ire1α and caspase-12 in spinal cord tissue were detected by immunohistochemistry,immunofluorescence and Western blot analysis at 1,4,8,16and 24 hours after ischemia-reperfusion.Results TUNEL staining showed that the number of apoptotic cells was gradually elevated with time.The expressions of Ire 1α and caspase-12 were increased at 1 hour after reperfusion,and peaked at 16 hours,but began to decline at 24 hours after reperfusion.The number of neurons with positive expressions of Irelaand caspase-12 was significantly higher than that of control group(P＜0.05).Conclusion Ire 1α and caspase-12 synergistically participate in the neuronal apoptosis induced by the endoplasmic reticulum stress.
