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Effect of elaidic acid on ABCA1 expression in raw 264.7 cells. Is it through PPAR-gamma?

机译:玉竹酸对未加工的264.7细胞中ABCA1表达的影响。是通过PPAR-gamma吗?

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摘要

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.
机译:近年来,反式脂肪酸已显示出与心血管疾病的强烈相关性。但是,解释其致动脉粥样硬化性的机制仍不清楚。参与胆固醇逆向转运途径的ABCA1被认为是心血管疾病的新治疗靶标。 PPAR-γ对巨噬细胞脂质稳态的影响的体外研究表明,PPAR-γ在调节ABCA1依赖性胆固醇向apoA-I途径的流出中具有作用。因此,在这项研究中,我们研究了作为最丰富的TFA的依地酸(EA)对RAW 264.7小鼠巨噬细胞系ABCA1和PPAR-γ表达的影响。因此,在使用MTT确定合适的EA浓度后,用不同浓度的EA处理RAW 264.7细胞,最后,通过实时PCR测定基因表达。我们的结果表明,在分别处理0.5、1和2 mM EA浓度的12 h后,与对照组相比,治疗组的ABCA1表达降低了1.7、2.3和5.1倍。此外,用EA处理24小时后,ABCA1表达下降的速率分别为2.1倍,2.6倍和5.7倍(P <0.01)。但是,EA对PPAR-γmRNA表达没有明显影响。因此,可以得出结论,EA的动脉粥样硬化作用可能是通过降低RAW 264.7细胞中ABCA1的表达来介导的。然而,这种降低并未通过改变PPAR-γ表达来介导。

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