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首页> 外文期刊>Journal of biochemical and molecular toxicology >Ca2+ Signaling and Cell Death Induced by Protriptyline in HepG2 Human Hepatoma Cells
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Ca2+ Signaling and Cell Death Induced by Protriptyline in HepG2 Human Hepatoma Cells

机译：普萘替林在HepG2人肝癌细胞中诱导Ca2 +信号传导和细胞死亡

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摘要

The effect of protriptyline on Ca2+ physiology in human hepatoma is unclear. This study explored the effect of protriptyline on [Ca2+](i) and cytotoxicity in HepG2 human hepatoma cells. Protriptyline (50-150M) evoked [Ca2+](i) rises. The Ca2+ entry was inhibited by removal of Ca2+. Protriptyline-induced Ca2+ entry was confirmed by Mn2+-induced quench of fura-2 fluorescence. Except nifedipine, econazole, SKF96365, GF109203X, and phorbol 12-myristate 13 acetate did not inhibit Ca2+ entry. Treatment with the endoplasmic reticulum Ca2+ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) inhibited 40% of protriptyline-induced response. Treatment with protriptyline abolished BHQ-induced response. Inhibition of phospholipase C (PLC) suppressed protriptyline-evoked response by 70%. At 20-40M, protriptyline killed cells which was not reversed by the Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N,N-tetraacetic acid-acetoxymethyl ester (BAPTA/AM). Together, in HepG2 cells, protriptyline induced [Ca2+](i) rises that involved Ca2+ entry through nifedipine-sensitive Ca2+ channels and PLC-dependent Ca2+ release from endoplasmic reticulum. Protriptyline induced Ca2+-independent cell death.
机译：曲普林对人肝癌中Ca2 +生理的影响尚不清楚。这项研究探讨了普鲁替林对人HepG2肝癌细胞中[Ca2 +]（i）和细胞毒性的影响。引起[Ca2 +]（i）的Protriptyline（50-150M）升高。通过除去Ca 2+抑制了Ca 2+的进入。普萘替林诱导的Ca2 +进入通过Mn2 +诱导的fura-2荧光猝灭来确认。除了硝苯地平，益康唑，SKF96365，GF109203X和佛波醇12-肉豆蔻酸酯13乙酸盐均不抑制Ca2 +的进入。内质网Ca2 +泵抑制剂2,5-二叔丁基对苯二酚（BHQ）的治疗抑制了40％的普替替林诱导的反应。普鲁替林治疗取消了BHQ引起的反应。抑制磷脂酶C（PLC）可将普罗替林诱发的反应抑制70％。在20-40M时，普鲁替林杀死了未被Ca2 +螯合剂1,2-双（2-氨基苯氧基）乙烷-N，N，N，N-四乙酸-乙酰氧基甲酯（BAPTA / AM）逆转的细胞。一起，在HepG2细胞中，普罗替林诱导的[Ca2 +]（i）升高，涉及通过硝苯地平敏感的Ca2 +通道进入Ca2 +以及从内质网释放PLC依赖性的Ca2 +。普罗替林诱导Ca2 +依赖性细胞死亡。

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