Abstract
In recent years, Trans Fatty Acids have shown a strong correlation with cardiovascular disease. However, the mechanisms explaining their atherogenicity are still unclear. ABCA1, which is involved in the reverse cholesterol transport pathway, has been considered as a new therapeutic target for cardiovascular disease. In vitro studies of the effects of PPAR-γ on lipid homeostasis in macrophage cells suggested a role for PPAR-γ in the regulation of ABCA1-dependent cholesterol efflux to apoA-I pathway. Thus, in this study we examined the effect of elaidic acid (EA) as the most abundant TFA on expression of ABCA1 and PPAR-γ in RAW 264.7 mouse macrophage cell line. Accordingly, after determining appropriate concentrations of EA using MTT, RAW 264.7 cells were treated with different concentrations of EA, and at the end, gene expression was assayed by Real-Time PCR. Our results shown that the expression of ABCA1 decreased in the treated group in comparison with the control group by 1.7, 2.3, and 5.1 fold, after 12 h treatment for 0.5, 1, and 2 mM EA concentration respectively. In addition, after 24 h treatment with EA, the rate of decreasing ABCA1 expression was 2.1, 2.6, 5.7 fold, respectively (P < 0.01). However, EA had no significant effect on PPAR-γ mRNA expression. Therefore, it could be concluded that the atherogenic effect of EA may be mediated by reducing ABCA1 expression in RAW 264.7 cells; however, this reduction has not mediated through altering PPAR-γ expression.