Resveratrol attenuates rotenone-induced inflammation and oxidative stress via STAT1 and Nrf2/Keap1/SLC7A11 pathway in a microglia cell line

Abstract

ScopeResveratrol 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. MethodsBV-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. ResultOur 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. ConclusionResveratrol 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.