Department of Physiology, School of Pre-Clinical Sciences, Guangxi Medical University, Nanning, Guangxi, China.
Qilu Medical University, Zibo, Shandong, China.
Biomed Res Int. 2020 Feb 25;2020:5080832. doi: 10.1155/2020/5080832. eCollection 2020.
Reducing cerebral ischemia-reperfusion injury is crucial for improving survival and neurologic outcomes after cardiac arrest/cardiopulmonary resuscitation (CA/CPR). The purpose of this study is to investigate the neuroprotective effects of green tea polyphenols (GTPs) concern with the modulation of endogenous antioxidation and endoplasmic reticulum stress.
After subjecting to CA/CPR, rats were randomized into the saline group (NS, = 40) and the GTPs group (GTPs, = 40) and the GTPs group (GTPs, = 40) and the GTPs group (GTPs.
Comparing with that in NS group, GTPs increased the expression of SOD1 and SOD2 at 12 h, 24 h, 48 h, 72 h, and the expression of GRP78 at 24 h and 48 h ( < 0.05) butdecreased caspase-12, CHOP, caspase-3 level, and apoptotic number of neurons ( < 0.05) butdecreased caspase-12, CHOP, caspase-3 level, and apoptotic number of neurons (.
GTPs exert neuroprotective effects via mechanisms that may be related to the enhancement of endogenous antioxidant capacity and inhibition of endoplasmic reticulum stress in CA/CPR rat models.
减轻脑缺血再灌注损伤对于改善心脏骤停/心肺复苏(CA/CPR)后患者的生存和神经功能结局至关重要。本研究旨在探讨绿茶多酚(GTPs)通过调节内源性抗氧化和内质网应激来发挥神经保护作用。
在发生 CA/CPR 后,大鼠随机分为盐水组(NS,n=40)和 GTPs 组(GTPs,n=40)。
与 NS 组相比,GTPs 组在 12 h、24 h、48 h 和 72 h 时 SOD1 和 SOD2 的表达增加,在 24 h 和 48 h 时 GRP78 的表达增加(<0.05),但 caspase-12、CHOP、caspase-3 水平和神经元凋亡数量降低(<0.05)。
GTPs 通过增强内源性抗氧化能力和抑制内质网应激来发挥神经保护作用,这可能与 CA/CPR 大鼠模型有关。