Li Huihua, Shen Yujun, Xiao Hui, Sun Wei
Department of Emergency Medicine, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, China.
Department of Pharmacology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Pathol Res Pract. 2021 Sep;225:153576. doi: 10.1016/j.prp.2021.153576. Epub 2021 Aug 12.
Resveratrol is abundant in grapes. A protective role for resveratrol in anti-oxidation and anti-inflammatory has been demonstrated. Rotenone is a pesticide, used to make animal models of Parkinson's disease (PD). The aim of our study was to investigate the protective effect of resveratrol on rotenone-induced microglial BV-2 cells and the mechanism.
BV-2 cells were pretreated with resveratrol for 1 h and then exposed to rotenone. The level of microglia activation was detected. The Iron content and the production of glutathione, malondialdehyde (MDA), reactive oxygen species(ROS) were detected to reflect the status of oxidative stress. The mRNA levels of interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) were measured by qRT-PCR.The expressions of p-STAT1, NF-E2-related factor (Nrf2), Kelch-like ECH-associated protein 1 (Keap1) and SLC7A11 were measured by western blot.
Our results showed that resveratrol attenuates microglia activation and M1 polarization in rotenone-induced BV-2 cells. Rotenone induced the production of free iron, ROS and MDA and inhibited the activity of glutathione, while the effects were reserved by resveratrol. Resveratrol also inhibited the induction effect of rotenone on IL-6, IL-1β, and TNF-α. In addition, resveratrol enhanced the protective effect of on rotenone-induced BV-2 cells via the inhibition of STAT1 and Keap1 and the upregulation of Nrf2 and SLC7A11.
Resveratrol attenuated rotenone-induced inflammation and oxidative stress in BV-2 cells through enhancing the inhibition of STAT1and Keap1 and the upregulation of Nrf2 and SLC7A11.
白藜芦醇在葡萄中含量丰富。白藜芦醇在抗氧化和抗炎方面的保护作用已得到证实。鱼藤酮是一种杀虫剂，用于制作帕金森病（PD）动物模型。本研究的目的是探讨白藜芦醇对鱼藤酮诱导的小胶质细胞BV-2细胞的保护作用及其机制。
用白藜芦醇预处理BV-2细胞1小时，然后暴露于鱼藤酮。检测小胶质细胞活化水平。检测铁含量、谷胱甘肽、丙二醛（MDA）、活性氧（ROS）的产生，以反映氧化应激状态。通过qRT-PCR检测白细胞介素-1β（IL-1β）、IL-6和肿瘤坏死因子-α（TNF-α）的mRNA水平。通过蛋白质免疫印迹法检测p-STAT1、核因子E2相关因子（Nrf2）、 Kelch样ECH相关蛋白1（Keap1）和溶质载体家族7成员11（SLC7A11）的表达。
我们的结果表明，白藜芦醇可减轻鱼藤酮诱导的BV-2细胞中小胶质细胞的活化和M1极化。鱼藤酮诱导游离铁、ROS和MDA的产生，并抑制谷胱甘肽的活性，而白藜芦醇可逆转这些作用。白藜芦醇还抑制鱼藤酮对IL-6、IL-1β和TNF-α的诱导作用。此外，白藜芦醇通过抑制STAT1和Keap1以及上调Nrf2和SLC7A11增强了对鱼藤酮诱导的BV-2细胞的保护作用。
白藜芦醇通过增强对STAT和Keap1的抑制以及Nrf2和SLC7A11的上调，减轻了鱼藤酮诱导的BV-2细胞中的炎症和氧化应激。
