白藜芦醇
小胶质细胞
神经毒性
药理学
免疫印迹
内质网
糖苷
莫里斯水上航行任务
化学
氧化应激
医学
免疫学
内分泌学
内科学
生物化学
炎症
海马体
毒性
立体化学
基因
作者
Yilong Yin,Guoguang Lv,Wang Zhang,Jing Yuan,Yuekui Yang,Yushui Wang,Shuai Liu,Shan Wang,Binbin Yan,Hai Bai,Chaoqun Ye
标识
DOI:10.1016/j.bbr.2023.114326
摘要
As a common complication of sepsis, sepsis-associated encephalopathy (SAE) is characterized by diffuse brain dysfunction and neurological damage and closely associated with long-term cognitive dysfunction. The dysregulated host response triggered by neurotoxicity of microglia is an important cause of diffuse brain dysfunction in SAE. Resveratrol glycoside has anti-inflammatory and antioxidant effects. However, there is no evidence whether resveratrol glycoside could alleviate SAE. LPS administration was used to induce SAE in mice. Step-down test (SDT) and Morris water maze test (MWM) were performed to evaluate the cognitive function of mice with SAE. Western blot and immunofluorescence were used to reveal the endoplasmic reticulum stress (ERS) regulation. Microglia cell line BV-2 was used to validate the effect of resveratrol glycoside on LPS-stimulated ERS in vitro. Compared with the control group, LPS-stimulated mice had decreased cognitive function, but this phenomenon was well reversed by resveratrol glycoside administration, in which the SDT assay showed longer retention time, both in short-term memory (STM) and long-term memory (LTM). Western blot indicated that the expression of ER stress-related protein PERK/CHOP in LPS-stimulated mice were significantly increased, while that in the resveratrol glycoside-treated group were relieved. Furthermore, Immunofluorescence revealed resveratrol glycoside mainly worked on microglia in mediating the ER stress, in which the expression of PERK/CHOP were significantly inhibited in resveratrol glycoside group mice. In vitro, BV2 showed consistent results with the aforementioned. Resveratrol glycoside could alleviate the cognitive dysfunction caused by LPS-induced SAE, mainly by inhibiting the ER stress and maintaining the homeostasis of ER function of microglia.
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