Desoxyrhaponticin attenuates M1 Macrophage Polarization via targeting PI3K/AKT/mTOR signaling pathway in RAW264.7 macrophage cells

Background: Macrophages play a critical role in the inflammatory response and excessive activation of M1-type macrophages is detrimental to the repair following acute myocardial infarction (AMI). Desoxyrhaponticin is an extract of Rheum tanguticum Maxim, a Chinese traditional nutrition food. Previous studies revealed that stilbene compounds of rhubarb possess anti-inflammatory activity, but no study has addressed whether Desoxyrhaponticin can regulate the polarization of macrophages to exert anti-inflammatory effects. Therefore, this study was designed to investigate the anti-inflammatory activity of Desoxyrhaponticin and the underlying mechanism. Methods: RAW264.7 cells were polarized to M1 macrophage by lipopolysaccharide (LPS). A cell counting kit-8 (CCK-8) assay was used to assess the cytotoxicity of Desoxyrhaponticin. Quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) and Western blotting were used to determine the mRNA and protein expression level of M1 macrophage marker. Western blotting was used to evaluate the activation of the PI3K/AKT/mTOR signaling pathway. PI3K inhibitor LY294002 were used to inhibit PI3K/AKT/mTOR signaling pathway. Results: The obtained results revealed that Desoxyrhaponticin inhibits the M1 polarization of RAW264.7 macrophages via the PI3K/AKT/mTOR signaling pathway. Conversely, PI3K inhibition by LY294002 exacerbated RAW264.7 macrophages polarization to the M1 type. Conclusion: Our study demonstrated the anti-inflammatory effects of Desoxyrhaponticin via PI3K/AKT/mTOR signaling pathway downregulation in RAW264.7 macrophages.