《Chinese Journal of Rehabilitation Theory and Practice》

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Protective Effect of Ser473-Akt Phosphorylation Mediated Atorvastatin on Cerebral Ischemia -reperfusion Injury in Rats

TAO Xi1, LU Wei2, HU Zhi-ping2, SONG Tao1, DENG Jing-gui1, CAI Hua-an1, WANG Shu-ling1, LIU Jia1   

  1. 1. Department of Rehabilitation Medicine, Mawangdui Hospital of Hunan Province, Changsha, Hunan 410016, China; 2. the Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China
  • Published:2016-06-25 Online:2016-07-04

Abstract: Objective To investigate the effect of Ser473-Akt phosphorylation in the protection of atorvastatin to cerebral ischemia-reperfusion (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 reperfusion. All rats were sacrificed 72 hours after reperfusion. HE staining and TUNEL staining were performed in the brain specimens. The expression 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 significantly 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.

Key words: cerebral ischemia-reperfusion, Ser473-Akt, phosphorylation, atorvastatin, apoptosis, rats