作者: Wenji Xie , Wenqin Xie , Zhenming Kang , Changcheng Jiang , Naizhen Liu
DOI: 10.1016/J.NEULET.2018.09.029
关键词: Pharmacology 、 Oxidative stress 、 Signal transduction 、 Western blot 、 PI3K/AKT/mTOR pathway 、 Cell 、 Hydromorphone 、 Hippocampal formation 、 Apoptosis 、 Chemistry 、 General Neuroscience
摘要: Abstract Hydromorphone has been shown to play protective effect in rat glial cell. However, whether hydromorphone plays important roles ischemia–reperfusion (IR) injury and the involved signaling pathway remains unclear. In this study, we detected HM IR mouse model, further followed by mechanism exploration. Preconditioning with was performed for continuous 4 days at doe of 2 mg/kg before induction. Intraperitoneal injection rapamycin (Rapa) administrated examine role mTOR injury. The mRNA expression level RT-PCR, protein western blot. Latency time apoptosis hippocampal CA1 neurons were 72 h after significantly increased time, decreased suppressed induced oxidative stress. Mechanically, preconditioning Bcl-2 p-mTOR levels Bax levels. Rapa administration reverses protecting from protect via activating pathway.