多不饱和脂肪酸对肝细胞α-氨基-β-羧酸酯-ε-半醛脱羧酶的下调不是由PPARα介导的

Naho Sasaki, Yukari Egashira, Hiroo Sanada
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摘要

饲粮多不饱和脂肪酸(PUFA)对大鼠肝脏α-氨基-β-羧酸-ε-半醛脱羧酶(ACMSD) [ec4.1.45]活性及mRNA水平的影响。本研究采用原代培养的大鼠肝细胞,研究PUFA下调ACMSD mRNA是否涉及ppar α介导的机制。从大鼠身上分离的原代培养肝细胞用脂肪酸、wy - 14643(一种PPARα激动剂)和/或MK-886(一种PPARα拮抗剂)孵育。采用竞争RT-PCR法检测ACMSD和酰基辅酶a氧化酶(ACO)作为过氧化物酶体标记酶的mRNA水平。这些结果提示PUFA对ACMSD mRNA水平的下调机制与wy - 14643不同,表明PUFA可能通过ppar α介导的途径以外的其他途径调控ACMSD mRNA水平。
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Down-regulation of α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase by polyunsaturated fatty acids in hepatocytes is not mediated by PPARα

Dietary polyunsaturated fatty acid (PUFA) suppresses hepatic α-Amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) [EC4.1.1.45] activity and mRNA level in rats. In this study, to examine whether down-regulation of ACMSD mRNA by PUFA involves PPARα-mediated mechanism or not, we investigated the effect of PUFA on the ACMSD level by using primary cultured rat hepatocytes. The primary cultured hepatocytes which were isolated from rats were incubated with fatty acids, WY-14,643 (a PPARα agonist) and/or MK-886 (a PPARα antagonist). ACMSD and acyl-CoA oxidase (ACO) as peroxisome marker enzyme mRNA level levels were determined by competitive RT-PCR method. These results lead us to the conclusion that the mechanism of decreased level of ACMSD mRNA by PUFA was different from that by WY-14,643, suggesting that there would be pathways other than a PPARα-mediated one for PUFA to regulate ACMSD mRNA level.

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