IDDF2019-ABS-0080 Rosiglitazone alleviates LPS-induced inflammation in RAW264.7 cells via the inhibition of NF-κB in A PPARγ-dependent manner

Abstract

Background Rosiglitazone is a synthetic peroxisome proliferator-activated receptor γ (PPARγ) agonist that is widely used to treat type 2 diabetes, recent research has highlighted its anti-inflammatory activity. The aim of this study was to investigate whether rosiglitazone can alleviate the decline in RAW264.7cells viability due to lipopolysaccharide(LPS) induced inflammation and the underlying mechanism. Methods RAW264.7 macrophages were stimulated with 100 ng/ml LPS to establish an inflammatory injury model. Cells were treated with LPS and various concentrations of rosiglitazone. Cell viability was assessed by MTT assays. Inflammatory cytokines were detected by ELISA and qRT-PCR.Nitric Oxide(NO) production was accessed using the Griess reagent system. The expression levels of key proteins in the NF-κB pathway were detected by western blotting. Results Rosiglitazone alleviated the decline in RAW264.7 cells viability induced by LPS and inhibited inflammatory cytokine expression in a concentration-dependent manner. Rosiglitazone significantly inhibited the upregulation of p65 phosphorylation and the downregulation of IκBα induced by LPS. The inhibitory effects could be blocked by PPARγ knockdown. Conclusions Our findings extend the application of rosiglitazone by demonstrating that it significantly inhibits the LPS induced inflammatory response in RAW264.7 macrophages via PPARγ activation and NF-κB suppression.