Protective Effect of Ser473-Akt Phosphorylation Mediated Atorvastatin on Cerebral Ischemia-reperfusion Injury in Rats
10.3969/j.issn.1006-9771.2016.06.007
- VernacularTitle:Ser473-Akt磷酸化介导阿托伐他汀保护大鼠脑缺血再灌注损伤
- Author:
Xi TAO
;
Wei LU
;
Zhiping HU
;
Tao SONG
;
Jinggui DENG
;
Huaan CAI
;
Shuling WANG
;
Jia LIU
- Publication Type:Journal Article
- Keywords:
cerebral ischemia-reperfusion;
Ser473-Akt;
phosphorylation;
atorvastatin;
apoptosis;
rats
- From:
Chinese Journal of Rehabilitation Theory and Practice
2016;22(6):655-659
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of Ser473-Akt phosphorylation in the protection of atorvastatin to cerebral ischemia-re-perfusion (I/R) injury in rats. Methods Forty male Sprague-Dawley rats were randomly divided into normal group (n=10), sham group (n=10), I/R group (n=10) and intervention group (n=10). A model of cerebral ischemia-reperfusion in rats was establishied, with ischemia for 2 hours and reperfusion for 72 hours. The normal group and the sham group received no injury. I/R group was administered with normal saline only, and the intervention group received atorvastatin 10 mg/kg prepared with normal saline at palinesthesia, 24 and 48 hours after reperfu-sion. All rats were sacrificed 72 hours after reperfusion. HE staining and TUNEL staining were performed in the brain specimens. The ex-pression of Akt and Ser473-Akt in the prefrontal cortex of the brain were detected with Western blotting. Results Compared with I/R group, 72 hours after reperfusion, the damage of nerve cells significantly lessened in the intervention group;the apoptosis positive cells significant-ly reduced in the intervention group (t=-6.014, P<0.001). The expression of Ser473-Akt in prefrontal cortex was higher in I/R group than in the normal group and the sham group (t>20.327, P<0.001), and was higher in the intervention group than in I/R group (t=3.649, P=0.007). Conclusion The Ser473-Akt phosphorylation plays an important role in the protection of atorvastatin in nerve cell through anti-apoptosis of nerve cells, and reducing cerebral I/R injury.
