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首页> 外文期刊>Cell biology international. >Caspase pathway of elaidic acid (9t-C18:1)-induced apoptosis in human umbilical vein endothelial cells
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Caspase pathway of elaidic acid (9t-C18:1)-induced apoptosis in human umbilical vein endothelial cells

机译：亚麻酸（9t-C18：1）诱导的人脐静脉内皮细胞凋亡的半胱天冬酶途径

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Although TFAs (trans fatty acids) do have effects on many endothelial functions, systemic inflammation and immune disorders, only limited experimental evidence is available that TFAs participate in the pathogenesis of endothelial cell apoptosis. HUVEC (human umbilical vein endothelial cells) were grown in medium with elaidic acid (9t-C18:1) at 50, 100, 200 and 400 mmol/l for 24 h. Apoptosis was measured by flow cytometry, and caspase 3, 8 and 9 activities by colorimetric assay and their mRNA expression by qRT-PCR (quantitative real-time PCR). Results showed that 9t-C18:1 induced apoptosis of HUVEC in a dosedependent manner. The activities and mRNA expression of caspases 8, 9 and 3 were significantly increased compared with that of the control. Z-IETD-FMK and Z-LEHD-FMK inhibited the activation of caspase 3 and apoptosis induced by 9t-C18:1. Also Z-IETD-FMK inhibited the activation of caspase 9. mRNA expressions of Bid and Smac (second mitochondria-derived activator of caspase)/DIABLO [direct IAP (inhibitor of apoptosis)-binding protein with low pI] were also significantly elevated. We conclude that 9t-C18:1 induces apoptosis of HUVEC through activating caspases 8, 9 and 3. The death receptor pathway and the mitochondrial pathway both participated in the apoptosis course induced by 9t-C18:1.
机译：尽管TFA（反式脂肪酸）确实对许多内皮功能，全身性炎症和免疫功能紊乱有影响，但只有有限的实验证据表明TFA参与了内皮细胞凋亡的发病机制。将HUVEC（人脐静脉内皮细胞）在含有依地酸（9t-C18：1）的培养基中以50、100、200和400 mmol / l的浓度培养24小时。通过流式细胞术测量凋亡，通过比色测定法测量胱天蛋白酶3、8和9的活性，并通过qRT-PCR（定量实时PCR）测量它们的mRNA表达。结果显示9t-C18：1以剂量依赖性方式诱导HUVEC的凋亡。与对照相比，胱天蛋白酶8、9和3的活性和mRNA表达显着增加。 Z-IETD-FMK和Z-LEHD-FMK抑制9t-C18：1诱导的caspase 3活化和凋亡。 Z-IETD-FMK也抑制caspase 9的激活。Bid和Smac（第二个线粒体衍生的caspase激活剂）/ DIABLO [pIA低的直接IAP（凋亡抑制剂）结合蛋白]的mRNA表达也显着升高。我们得出的结论是9t-C18：1通过激活胱天蛋白酶8、9和3诱导HUVEC凋亡。死亡受体途径和线粒体途径均参与了9t-C18：1诱导的凋亡过程。

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