神经传染病

抽象的

Triptolide Protects Neurons from Endoplasmic Reticulum Stress-Mediated Apoptosis in Cerebral Ischemic Injury Rats

Yingchao Su, Benping Zhang, Yihong Ma, Yongzhi San, Jun Qi, Chunhua Liu, Senlin Mao, Mingjie Li, Pengwei Wang and Feng Li

This study aimed to investigate the neuroprotective effect of Triptolide (T10) on cerebral ischemia/reperfusion (I/R) injury and explore the underlying mechanisms. Adult male Sprague-Dawley rats were treated with T10 and subjected to middle cerebral artery occlusion (MCAO) for 90 min. Neurological deficits and infarct volume were measured 24 h after reperfusion. ER stress-mediated proteins, ryanodine receptors (RyRs), cysteinyl aspartate specific proteinase 8 (Caspase-8), Fas-associated death domain (FADD) and C/EBP homologous protein (CHOP) were evaluated 1, 4, and 24 h after reperfusion. Pretreatment with 1 mg/kg of T10 significantly reduced infarct volume and neurological deficits. Further, TUNEL staining demonstrated T10 significantly decreased neuronal apoptosis in the peri-infarct area after reperfusion. More importantly, T10 prevented ER stress-mediated expression of RyR, FADD, caspase-8 and CHOP in the peri-infarct area of rats. These results indicate that T10 attenuates the ER stress-induced apoptosis in cerebral I/R injury and suggest that T10 is a promising agent for the treatment of ischemic stroke.