Objective: To investigate whether the combination of HDL and miR-33 in patients with acute coronary syndromes(ACS) could impair function of HDL. Methods: 48 ACS patients were enrolled as the ACS group, and 52 healthy subjects as the control group. HDL was separated and purified as large, medium and small particles from the two groups. Real-time fluorescent quantitative PCR was performed to detect the expression levels of each sub-fraction and plasma miR-33. In vitro, experiment groups included:negative control group, rHDL group, large HDL particle(L-HDL) group, medium HDL particle group, small HDL particle group and L-HDL+anti-miR33 group. 3H labeled cholesterol was used to detect intracellular cholesterol efflux and the Luminex 200 kit was used to detect the expression of inflammatory factors in THP-1 foam cells. Results: The study showed that the levels of miR-33 in the plasma and each sub-fraction of HDL of ACS patients were overall increased significantly, especially in L-HDL. Compared with the control group, the cellular cholesterol efflux capacity and anti-inflammatory capacity of each sub-fraction of HDL in ACS patients were significantly impaired. After inhibiting the combination between miR-33 and HDL, the cholesterol efflux ability and anti-inflammatory ability of L-HDL were partly restored. Conclusion: In the acute inflammatory state of ACS, the level of miR-33 combined with HDL was up-regulated, leading to the dysfunctional HDL which antiatherogenic function has been impaired.
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