Ji Kangxiang, Xue Long, Cheng Jiwei, Bai Yu
Department of Neurology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, China.
Department of Neurosurgery, Yangpu Hospital, Tongji University School of Medicine, Shanghai 200090, China.
Brain Res Bull. 2016 Mar;121:68-74. doi: 10.1016/j.brainresbull.2015.12.007. Epub 2016 Jan 6.
It is of great importance to protect the brain against cerebral ischemia and reperfusion (I/R) injury, which leads to excitotoxicity, redox imbalance, inflammation and apoptosis; however, there is currently no effective treatment. The present study aimed to investigate the effect of H2S preconditioning on cerebral I/R injury and its underlying mechanism. The results demonstrated that H2S preconditioning significantly prevented the development of neurological function abnormality, inflammation and oxidative injury in mice as well as cognitive impairment caused by cerebral I/R. H2S preconditioning also suppressed the apoptosis caused by cerebral I/R. Moreover, the protective effect of H2S preconditioning was found to involve heat shock protein 70 (HSP70), in which the PI3K/Akt/Nrf2 pathway was involved. The data showed that H2S preconditioning could protect mice against cerebral I/R injury by the induction of HSP70 and the PI3K/Akt/Nrf2 pathway.
保护大脑免受脑缺血再灌注(I/R)损伤至关重要,这种损伤会导致兴奋性毒性、氧化还原失衡、炎症和细胞凋亡;然而,目前尚无有效的治疗方法。本研究旨在探讨硫化氢预处理对脑I/R损伤的影响及其潜在机制。结果表明,硫化氢预处理可显著预防小鼠神经功能异常、炎症和氧化损伤的发展,以及脑I/R引起的认知障碍。硫化氢预处理还可抑制脑I/R引起的细胞凋亡。此外,发现硫化氢预处理的保护作用涉及热休克蛋白70(HSP70),其中PI3K/Akt/Nrf2信号通路参与其中。数据表明,硫化氢预处理可通过诱导HSP70和PI3K/Akt/Nrf2信号通路保护小鼠免受脑I/R损伤。