Background Systemic lupus erythematosus (SLE) is the autoimmune disease that patients with chronic inflammatory phenomena can induce early atherosclerosis, thereby increasing the risk of cardiovascular disease.
Objectives The aim of this study was to investigate the peroxisome proliferator-activated receptor γ (PPAR γ)- liver X receptors α (LXRα)-ATP binding cassette transporter-A1 (ABCA1) pathway in reverse cholesterol transport and its association with cholesterol removal factors including lecithin cholesterol acyltransferase (LCAT), cholesteryl ester transfer protein (CETP) and ABCA1.
Methods A total of 68 subjects including thirty-eight SLE patients and thirty healthy subjects participated in this study. PPARα, PPARγ, LXRα and ABCA1 mRNA levels in peripheral blood mononuclear cells were analyzed by RT-PCR analysis and plasma levels of LCAT, CETP and ABCA1 were determined by enzyme-linked immunosorbent assay.
Results PPARα, PPARγ, LXRα, and ABCA1 mRNA levels of SLE patients were significantly lower than those in healthy controls. With respect to insulin resistance, patients with HOMA IR>2 had higher levels of glucose, insulin, and triglyceride (TG) than patients with HOMA IR<2. However, HOMA-IR values were not related to factors involved in cholesterol efflux in this study. In addition, total cholesterol (TC) levels were significantly correlated to CETP and LCAT. Plasma TG levels were significantly correlated to CETP, and high-density lipoprotein cholesterol (HDL-C) levels were significantly correlated to PPARα, CETP, and LCAT in patients with SLE. The PPARγ mRNA expression was much more associated with HDL-C than TC and TG. The plasma levels of lipids in SLE seemed to be more associated with PPARα, PPARγ, LXRα and ABCA1 mRNA expressions than plasma level of ABCA1.
Conclusions PPARα, PPARγ, LXRα and ABCA1 mRNA expressions were significantly decreased in SLE patients, suggesting the reduction of the reverse cholesterol transport in terms of PPARγ-LXRα-ABCA1 pathway may at least in part play an important role in the risk of atherosclerosis in SLE.
Disclosure of Interest None declared
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