Liu Jing, Li Ying, Mei Chunli, Ning Xianbin, Pang Jinfeng, Gu Lei, Wu Liang
Neurology Department, Affiliated Hospital of Beihua University , Jilin, China.
Rehabilitation Center, Beijing Xiaotangshan Hospital , Beijing, China.
Biosci Biotechnol Biochem. 2020 Jul;84(7):1401-1408. doi: 10.1080/09168451.2020.1754158. Epub 2020 Apr 14.
Cerebral ischemia reperfusion (I/R) is a therapeutic strategy for ischemia; however, it usually causes injury by the aspect of inflammation and neuron apoptosis. This investigation aims to investigate the protective effects of phytic acid (IP6) for cerebral I/R injury in vitro. PC-12 cells under Oxygen and glucose deprivation/reperfusion (OGD/R) were performed to mimic cerebral I/R. IP6 was pretreated before PC-12 cells under OGD/R treatment. The data showed that IP6 activated the expression of sestrin2 in OGD/R injured PC-12 cells. IP6 inhibited OGD/R induced inflammation, oxidative stress, and apoptosis by activating sestrin2. Besides, p38 MAPK may mediate the effects of sestrin2 activated by IP6. Therefore, IP6 can be a potential drug to prevent neurological damage in cerebral I/R injury.
脑缺血再灌注（I/R）是一种针对缺血的治疗策略；然而，它通常会在炎症和神经元凋亡方面导致损伤。本研究旨在探讨肌醇六磷酸（IP6）在体外对脑I/R损伤的保护作用。采用氧糖剥夺/再灌注（OGD/R）处理PC-12细胞以模拟脑I/R。在对PC-12细胞进行OGD/R处理之前，先对其进行IP6预处理。数据显示，IP6可激活OGD/R损伤的PC-12细胞中sestrin2的表达。IP6通过激活sestrin2抑制OGD/R诱导的炎症、氧化应激和细胞凋亡。此外，p38丝裂原活化蛋白激酶（p38 MAPK）可能介导IP6激活sestrin2的作用。因此，IP6可能是一种预防脑I/R损伤中神经损伤的潜在药物。
