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Upregulation of Fas and FasL expression in nicotine-induced apoptosis of endothelial cells.

机译:烟碱诱导的内皮细胞凋亡中Fas和FasL表达的上调。

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摘要

Although smoking-related coronary vascular disease is well documented, the effects of nicotine have not been fully investigated. There is controversy over reports about the effect of nicotine on apoptosis. The effect of nicotine on apoptosis of human umbilical vein endothelial cells (HUVECs) and the expressions of Fas/Fas ligand (FasL) and caspase-3 were evaluated in this study. Annexin V fluorescein isothiocyanate and propidium iodide double staining demonstrated that nicotine (0.2 microM, 0.5 microM and 1 microM) could induce apoptosis of HUVECs; reverse transcription (RT)-PCR and Western blotting analysis demonstrated that levels of Fas and FasL expression were increased in nicotine-treated HUVECs. Moreover, caspase-3 expression was also increased. These data indicate that nicotine induces the apoptosis of HUVECs, and that the Fas/FasL pathway may play an important role. This provides evidence that nicotine may have an important role in cardiovascular pathology and atherogenesis.
机译:尽管与吸烟有关的冠状动脉疾病已有充分文献记载,但尼古丁的影响尚未得到充分研究。关于尼古丁对细胞凋亡的影响的报道存在争议。本研究评估了尼古丁对人脐静脉内皮细胞(HUVEC)凋亡的影响以及Fas / Fas配体(FasL)和caspase-3的表达。 Annexin V异硫氰酸荧光素和碘化丙啶双重染色表明,尼古丁(0.2 microM,0.5 microM和1 microM)可以诱导HUVEC凋亡。逆转录(RT)-PCR和Western印迹分析表明,尼古丁治疗过的HUVEC中Fas和FasL表达水平增加。此外,caspase-3表达也增加。这些数据表明尼古丁可诱导HUVEC的凋亡,而Fas / FasL途径可能起重要作用。这提供了尼古丁可能在心血管病理和动脉粥样硬化中起重要作用的证据。

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