Heat shock protein expression affects high-density lipoprotein function in atherosclerosis

High-density lipoprotein (HDL) and heat shock protein (HSP) play important role in atherosclerosis (AS) lesion. This study aimed to investigate the relationship between HDL function and HSP65 in AS by observing different doses of HSP65 impact on macrophage cholesterol efflux rate in apolipoprotein E gene deleted mice and HDL anti-inflammatory, antioxidant function. Healthy male ApoE(-/-) mice at 8 weeks were fed with high-fat diet. On the 16th week, blood lipid, serum IFN-gamma, IL-10, MPO, PON1 levels were tested. HSP65 antibody titer and peritoneal macrophages H-3-TC switching-out rate were determined. Liver tissue ABCA1, ABCG1, SR-BI, and LXR-alpha protein expression were detected by Western blot. TG, TC, and LDL-C level elevated, while HDL-C decreased significantly in group B, C, D, and E compared with group A (P < 0.05). Group E showed lower HDL-C level than group B (P < 0.05). HSP65 antibody titer, IFN-gamma, and IL-10 level in group B were similar to group A (P < 0.05). HSP65 antibody titer and IFN-gamma level increased, whereas IL-10 reduced in group C, D, and E compared with group B with dose-dependent (P < 0.05). Macrophages H-3-TC switching-out rate, PON1 activity, and liver tissue ABCA1, ABCG1, SR-BI, and LXR-alpha protein level declined obviously, while MPO activity increased significantly in group B, C, D, E compared with group A (P < 0.05). HSP65 induced inflammatory immunoreaction, damaged HDL function, and declined macrophage cholesterol efflux rate through downregulating liver tissue ABCA1, ABCG1, SR-BI, and LXR-alpha protein with dose-dependent.