Mechanism of resveratrol inhibiting monosodium urate induced oxidative damage of RAW264.7 macrophages

The aim of this research is to investigate the effects of resveratrol on the inflammatory factors, oxidative stress indexes and the related genes of nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in RAW264.7 macrophages induced by monosodium urate (MSU) and to provide a theoretical basis for the treatment of acute gouty arthritis (AGA). Different concentrations of resveratrol were used to treat RAW264.7 cells for 5 hours, then MSU was added to stimulate them for 24 hours. The proliferation of RAW264.7 cells were detected by CCK-8 method. The level of tumor necrosis factor α secreted by cells were detected by ELISA method. The content of reaction oxygen species (ROS) in cells were detected by 2',7'-dichlorodi-hydrofluorescein diacetate (DCFH-DA) probe method. The contents of superoxide dismutase (SOD) and malonaldehyde (MDA) in cells were detected by the kits. The expression of Nrf2, Kelch like ECH related protein 1 (Keap1), NAD(P)H quinone oxidoreductase 1 (NQO1), HO-1 mRNA were detected by real time PCR method. The results showed that resveratrol could inhibit the proliferation of RAW264.7 cells, significantly inhibit the TNF-α level of RAW264.7 cells induced by MSU, significantly inhibit the expression of ROS and MDA, and increase the expression of SOD in RAW264.7 cells induced by MSU. Resveratrol could reduce the expression of Keap1 mRNA in RAW264.7 cells induced by MSU, and increase the expression of Nrf2, NQO1, HO-1 mRNA. It is suggested that resveratrol can inhibit the inflammatory response of RAW264.7 macrophages induced by MSU, and improve the antioxidant capacity of macrophages by regulating Nrf2/HO-1 signal pathway.