کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2601622 1133335 2006 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Naringenin-induced apoptosis via activation of NF-κB and necrosis involving the loss of ATP in human promyeloleukemia HL-60 cells
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
Naringenin-induced apoptosis via activation of NF-κB and necrosis involving the loss of ATP in human promyeloleukemia HL-60 cells
چکیده انگلیسی

Naringenin (NGEN), a flavonoid, has shown cytotoxicity in various human cancer cell lines and inhibitory effects on tumor growth. In this study, we investigated the apoptosis induced by NGEN via the activation of NF-κB and necrosis involving the loss of ATP in human promyeloleukemia HL-60 cells. Exposure to NGEN induced apoptosis dose-dependently up until 0.5 mM, but not at 1 mM as demonstrated by a quantitative analysis of nuclear morphological change and flow cytometric analysis. An extensive inhibitor for caspases, abolished the NGEN-induced apoptosis. The apoptosis-triggering concentration of NGEN was shown to markedly promote the activation of caspase-3, and slightly promote that of caspase-9, but had no effect on caspase-8. NGEN-induced apoptosis caused by induction of specific NF-κB-binding activity and involving the degradation of IκBα. Incubation with a high concentration of NGEN (1 mM) reduced intracellular ATP levels, but no change was observed at lower concentrations. NGEN increased dose-dependently hyperpolarization of mitochondrial membrane potential. This result indicates a common pathway to apoptosis and necrosis by NGEN. One of the mechanisms by NGEN-induced apoptosis may relate to the activation of NF-κB that correlates with degradation of IκBα. Induction of necrosis by NGEN suggests causing by intracellular ATP depletion and mitochondria dysfunctions.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology Letters - Volume 166, Issue 2, 10 October 2006, Pages 131–139
نویسندگان
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