Silencing p62 reduces ox-LDL-induced M1 polarization and inflammation in macrophages by inhibiting mTOR/NF-κB signaling pathways

Macrophages can change their phenotypes according to the changes in microenvironment, and thus have various functions, that is, macrophages polarization. Macrophage phenotype is associated with progression of atherosclerotic plaques. Studies shown a large accumulation p62 protein Whether affects level macrophage polarization inflammation its mechanism not clear. The levels treated ox-LDL were detected by western blotting qRT-PCR. Several polarizing markers cytokines atherosclerosis blotting, ELISA, qRT-PCR, flow cytometry assess phenotype. effect on treatment was studied silencing gene technique. activity mTOR NF-κB signaling pathways evaluated detecting p-mTOR intranuclear p65 explore p62. Rapamycin inhibited demonstrate role activating pathway therapy induced M1 macrophages. significant increase an inflammatory cytokines. After silencing, decreased significantly, while M2 anti-inflammatory increased significantly. Silencing nuclear translocation. ox-LDL-induced translocation markers, markers. induces through mTOR/NF-κB pathway.