کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5738603 1615064 2016 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Research articleEffects of 4-phenyl butyric acid on high glucose-induced alterations in dorsal root ganglion neurons
ترجمه فارسی عنوان
مقاله پژوهشی اثرات اسید 4-فنیل بوتیریک بر تغییرات ناشی از گلوکز بالا در نورون های گانگلیونی ریشه
کلمات کلیدی
نوروپاتی دیابتی، گانگلیون ریشه پشتی، هیپرگلیسمی، ادراک درد، بیان کانال سدیم،
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
چکیده انگلیسی


- Pathways involving in diabetic neuropathy are still not fully understood.
- ER stress could be triggered by hyperglycemia in primary sensory neurons.
- Hyperglycemia-induced alteration may be blocked by the 4-phenyl butyric acid.

Mechanisms and pathways involving in diabetic neuropathy are still not fully understood but can be unified by the process of overproduction of reactive oxygen species (ROS) such as superoxide, endoplasmic reticulum (ER) stress, downstream intracellular signaling pathways and their modulation. Susceptibility of dorsal root ganglion (DRG) to internal/external hyperglycemic environment stress contributes to the pathogenesis and progression of diabetic neuropathy. ER stress leads to abnormal ion channel function, gene expression, transcriptional regulation, metabolism and protein folding. 4-phenyl butyric acid (4-PBA) is a potent and selective chemical chaperone; which may inhibit ER stress. It may be hypothesized that 4-PBA could attenuate via channels in DRG in diabetic neuropathy. Effects of 4-PBA were determined by applying different parameters of oxidative stress, cell viability, apoptosis assays and channel expression in cultured DRG neurons. Hyperglycemia-induced apoptosis in the DRG neuron was inhibited by 4-PBA. Cell viability of DRG neurons was not altered by 4-PBA. Oxidative stress was significantly blocked by the 4-PBA. Sodium channel expression was not altered by the 4-PBA. Our data provide evidence that the hyperglycemia-induced alteration may be reduced by the 4-PBA without altering the sodium channel expression.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 635, 2 December 2016, Pages 83-89
نویسندگان
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