کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2200714 1551308 2014 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Casein kinase 2 inhibition attenuates cholesterol oxidation product-induced apoptosis by suppressing the activation of the mitochondrial pathway and the caspase-8- and bid-dependent pathways
ترجمه فارسی عنوان
مهار کردن کازئین کیناز 2 باعث کاهش اپی پوسیدگی ناشی از اکسیداسیون کلسترول توسط سرکوب فعال شدن مسیر میتوکندریال و مسیرهای وابسته به کاسپاز 8- و پیشنهاد می شود
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
چکیده انگلیسی


• Casein kinase 2 inhibition.
• Inhibits formation of reactive oxygen species and depletion of GSH.
• Suppresses the mitochondrial pathway and the caspase-8- and bid-dependent pathways.
• Attenuates cholesterol oxidation product-induced apoptosis in PC12 cells.

Protein casein kinase 2 is involved in signal transduction, cell growth and apoptosis. However, it is unclear whether the cholesterol oxidation product-induced cell death is regulated by casein kinase 2. Therefore, in the respect of the cell death process, we assessed the regulatory effect of the casein kinase 2 on the cholesterol oxidation product-induced apoptosis in neuronal cells using differentiated PC12 cells. Casein kinase 2 inhibitors (4,5,6,7-tetrabromobezotriazole (TBB) and apigenin) which do not have toxic effects, reduced the 7-ketocholesterol or 25-hydroxycholesterol-induced cell death and nuclear damage in PC12 cells. Treatment with TBB inhibited the 7-ketocholesterol-induced decrease in Bid, Bcl-2 and survivin protein levels, increase in Bax levels, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), cleavage of PARP-1, and increase in the tumor suppressor p53 levels. The results showed that the casein kinase 2 inhibitor at the concentrations tested which does not induce toxic effects, may attenuate the cholesterol oxidation product-induced apoptosis in differentiated PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The preventive effect appears to be ascribed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 65, January 2014, Pages 30–39
نویسندگان
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