Effect of Le ’ermai Capsule on Protein Expression of HO- 1，SOD1，SOD2 and Nrf 2 in the Cerebral Cortex of Cerebral Ischemia/Reperfusion Injury Rats / 中国药房

ABSTRACT

OBJECTIVE： To study the effects and mechanism of Le’ermai capsule on oxidative stress injury in the cerebral cortex of cerebral ischemia-reperfusion injury rats. METHODS： Totally 65 rats were randomly divided into sham operation group （normal saline）， model group （normal saline）， positive control group （Naoxintong capsule， 3.40 g/kg）， Le’ermai capsule high-dose and low-dose groups （0.37， 0.18 g/kg）， with 13 rats in each group. Except that sham operation group received sham operation， and middle cerebral artery occlusion/reperfusion （MCAO/R） model was induced by suture-occluded method. 24 h after modeling， they were given relevant medicine intragastrically， once a day， for consecutive 7 d. 2 h after last administration， cerebral ischemic area was determined by TTC staining. The pathological changes of cerebral tissue were observed by HE staining. The protein expressions of HO-1， SOD1， SOD2 and Nrf2 in cerebral cortex were detected by Western blot assay. RESULTS： Compared with sham operation group， the area of cerebral ischemic was increased significantly in model group（P＜0.05）， interstitial edema was serious， inflammatory cell infiltration increased significantly； and the protein expression levels of HO-1 and SOD1 in cortex tissue were significantly increased （P＜0.05）， and the protein expression levels of SOD2 and Nrf2 were significantly decreased （P＜0.05）. Compared with model group， the area of cerebral ischemic area of Le’ermai capsule high-dose and low-dose groups were significantly decreased （P＜0.05）. The interstitial edema， inflammatory cell infiltration and microcytes proliferation were decreased. The protein expression levels of HO-1， SOD1， SOD2 and Nrf2 in the cerebral cortex tissue were significantly increased （P＜0.05）. CONCLUSIONS：Le’ermai capsule can improve cerebral ischemia/reperfusion injury to certain extent， and which may be associated with up-regulating the protein expression of antioxidant factors HO-1， SOD1， SOD2 and Nrf2 in the cortex.