Analgecine protects against cerebral ischemia-reperfusion through apoptosis inhibition and anti-neuroinflammation in rats

Abstract

Stroke influence the quality of life of patients and leave big public health issues as acute cerebrovascular disease all over the world. Analgecine (AGC) relieves pain and accelerates repair of nerve injury. This current study aims to observe the pharmacological effects and related mechanisms of AGC in cerebral ischemic stroke among middle cerebral artery ischemia-reperfusion (MCAO) rats. After seven days of AGC administration, motor function was enhanced as evidenced by the prehensile traction test. Morphological ameliorations were observed by immunohistochemistry analysis. The protein expression levels of HSP70, Bcl-2, Bax, TRAF-6, MyD88, BDNF, NGF, pCREB, CREB, pTrkB, TrkB, pAKT and AKT were estimated by western blot. Meanwhile, AGC alleviated MCAO-induced inflammation chiefly by decreasing inflammatory cytokines in rat brain tissues. These results above suggested that MCAO-caused brain infarction was obviously alleviated by AGC. The immunohistochemistry data showed that AGC reduced neuronal injury and apoptosis, and inhibited microglia and astrocytes activation. The protein results suggested the expression of apoptosis-relevant proteins decreased among AGC treated groups and the neurotrophin related proteins were obviously enhanced by CREB/BDNF/TrkB/AKT and HSP70/Bcl-2/Bax pathways. Collectively, the results demonstrated that AGC primarily promoted neuro-nutrition, reduced the injury of nerve apoptosis and ameliorated neuroinflammation. In summary, AGC played a neuroprotective role, which had provided reliable evidence for AGC to be a potential drug in treating stroke.