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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Protective Effects of Oleic Acid Against Palmitic Acid-Induced Apoptosis in Pancreatic AR42J Cells and Its Mechanisms
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Protective Effects of Oleic Acid Against Palmitic Acid-Induced Apoptosis in Pancreatic AR42J Cells and Its Mechanisms

机译：油酸对棕榈酸诱导的胰腺AR42J细胞凋亡的保护作用及其机制

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Palmitic acid (PAM), one of the most common saturated fatty acid (SFA) in animals and plants, has been shown to induce apoptosis in exocrine pancreatic AR42J cells. In this study, we investigated cellular mechanisms underlying protective effects of oleic acid (OLA) against the lipotoxic actions of PAM in AR42J cells. Exposure of cells to long-chain SFA induced apoptotic cell death determined by MTT cell viability assay and Hoechst staining. Co-treatment of OLA with PAM markedly protected cells against PAM-induced apoptosis. OLA significantly attenuated the PAM-induced increase in the levels of pro-apoptotic Bak protein, cleaved forms of apoptotic proteins (caspase-3, PARP). On the contrary, OLA restored the decreased levels of anti-apoptotic Bcl-2 family proteins (Bcl-2, Bcl-xL, and Mcl-1) in PAM-treated cells. OLA also induced up-regulation of the mRNA expression of Dgat2 and Cpt1 genes which are involved in triacylglycerol (TAG) synthesis and mitochondrial β-oxidation, respectively. Intracellular TAG accumulation was increased by OLA supplementation in accordance with enhanced expression of Dgat2 gene. These results indicate that restoration of anti-apoptotic/pro-apoptotic protein balance from apoptosis toward cell survival is involved in the cytoprotective effects of OLA against PAM-induced apoptosis in pancreatic AR42J cells. In addition, OLA-induced increase in TAG accumulation and up-regulation of Dgat2 and Cpt1 gene expressions may be possibly associated in part with the ability of OLA to protect cells from deleterious actions of PAM.
机译：棕榈酸（PAM）是动植物中最常见的饱和脂肪酸（SFA）之一，已显示出可诱导外分泌胰腺AR42J细胞凋亡。在这项研究中，我们调查了油酸（OLA）对AR42J细胞中PAM的脂毒性作用的保护作用的细胞机制。通过MTT细胞活力测定和Hoechst染色确定细胞暴露于长链SFA诱导的凋亡细胞死亡。 OLA与PAM共同处理可显着保护细胞免受PAM诱导的细胞凋亡。 OLA显着减弱了PAM诱导的促凋亡Bak蛋白，裂解形式的凋亡蛋白（caspase-3，PARP）水平的增加。相反，OLA恢复了PAM处理细胞中抗凋亡Bcl-2家族蛋白（Bcl-2，Bcl-xL和Mcl-1）的水平降低。 OLA还诱导Dgat2和Cpt1基因的mRNA表达上调，这些基因分别参与三酰基甘油（TAG）合成和线粒体β-氧化。根据Dgat2基因表达的增强，通过补充OLA可以增加细胞内TAG的积累。这些结果表明，从凋亡向细胞存活的抗凋亡/促凋亡蛋白平衡的恢复与OLA对PAM诱导的胰腺AR42J细胞凋亡的细胞保护作用有关。另外，OLA诱导的TAG积累增加以及Dgat2和Cpt1基因表达的上调可能与OLA保护细胞免受PAM有害作用的能力有关。

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