当社グループは 3,000 以上の世界的なカンファレンスシリーズ 米国、ヨーロッパ、世界中で毎年イベントが開催されます。 1,000 のより科学的な学会からの支援を受けたアジア および 700 以上の オープン アクセスを発行ジャーナルには 50,000 人以上の著名人が掲載されており、科学者が編集委員として名高い
。オープンアクセスジャーナルはより多くの読者と引用を獲得
700 ジャーナル と 15,000,000 人の読者 各ジャーナルは 25,000 人以上の読者を獲得
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.