TY -的A2 -汉拉罕,简非盟-张小燕盟——张,文献盟——见鬼,Zhancui盟——苏姗姗AU - Li Zhanqiang AU - Lu, Dianxiang PY - 2020 DA - 2020/06/10 TI -认知保护机制的藏红花素预处理大鼠急性提交高海拔缺氧暴露SP - 3409679六世- 2020 AB -在高海拔的地方氧气供应不足导致氧化应激,导致海马神经细胞退化和记忆障碍。在我们之前的研究中,我们发现,认知功能障碍发生在雄性SD大鼠迅速暴露在4200米高空的3天。我们还发现,藏红花素显示认知保护作用下缺氧通过调节SIRT1 / PGC-1 α通路在老鼠的海马。在本文中,专注于SIRT1 / PGC-1有关的因素 α途径,我们提出了进一步阐明藏红花素的药理机制。成年男性Sprague-Dawley老鼠被随机分为五组:对照组、缺氧组(老鼠迅速运送到高海拔4200米的72 h),和藏红花素+缺氧组(预处理藏红花素的25、50、100毫克/公斤/天为3天)。学习和记忆能力被莫里斯水迷宫测试分析。海马组织病理学变化观察到他染色和尼氏小染色。bcl - 2的表达NRF1、TFAM,伯灵顿,caspase-3通过免疫组织化学方法检测,rt - pcr和免疫印迹试验。内容的丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH),谷胱甘肽过氧化物酶和(GSHPx)检测到稍后通知,WST,比色法方法。神经细胞凋亡被TUNEL染色观察。藏红花素预处理后,旅行距离的比例明显减少,时间在目标象限被莫里斯水迷宫显著增加测试。和海马神经元的损伤也显著改善基于他染色和尼氏小染色。此外,在海马组织,线粒体biosynthesis-related NRF1因素,TFAM表达增加; oxidative stress factors of SOD, GSH, and GSHPx expression level were increased, and MDA and glutathione disulfide (GSSG) level were decreased; antiapoptotic protein Bcl-2 expression was increased, and proapoptotic proteins Bax and caspase-3 expression were decreased, with a manner of crocin dose dependent. Therefore, the cognitive protective mechanism of crocin in rat under acute hypoxia was related to promoting mitochondrial biosynthesis, ameliorating oxidative stress injury, and decreasing neuronal apoptosis. SN - 2314-6133 UR - https://doi.org/10.1155/2020/3409679 DO - 10.1155/2020/3409679 JF - BioMed Research International PB - Hindawi KW - ER -