کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5506801 | 1400303 | 2016 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Dehydroascorbic acid-induced endoplasmic reticulum stress and leptin resistance in neuronal cells
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کلمات کلیدی
IRE1protein kinase RNA (PKR)-like ER kinaseGRP78ATF6XBP1UPRDHAAC/EBP homologous protein - C / EBP پروتئین همولوگAscorbic acid - آسکوربیک اسیدEndoplasmic reticulum (ER) stress - استرس اندوتلیوم رتیکولوم (ER)Dehydroascorbic acid - اسید Dehydroascorbicincubation buffer - بافر انکوباتورCHOP - تکه کردنendoplasmic reticulum - شبکه آندوپلاسمی activating transcription factor 6 - فعال کردن عامل رونویسی 6Leptin - لپتین Leptin resistance - مقاومت لپتینUnfolded protein response - پاسخ پروتئین آشکارUnfolded protein response (UPR) - پاسخ پروتئین باز شده (UPR)X-box-binding protein 1 - پروتئین X-box binding 1glucose-regulated protein 78 - پروتئین تنظیم شده با گلوکز 78PERK - پرک
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Due to its anti-obesity effects, an adipocyte-derived hormone, leptin, has become important for the treatment of obesity. However, most obese subjects are in a state of leptin resistance, and endoplasmic reticulum (ER) stress is suggested to be involved in the pathophysiology of leptin resistance. Dehydroascorbic acid (DHAA), an oxidized form of vitamin C, was found to be increased in diabetes. In the present study, we investigated the possible effects of DHAA on the activation of ER stress and leptin resistance. A human neuroblastoma cell line, stably transfected with the Ob-Rb leptin receptor (SH-SY5Y-ObRb), was treated with DHAA. We found that DHAA upregulated ER stress-related genes such as GRP78, CHOP, and spliced XBP1. Moreover, leptin-induced STAT3 phosphorylation was hindered by DHAA. These results suggested that increases in the levels of DHAA might be harmful to neurons, contributing to defective leptin-responsive signaling.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 478, Issue 2, 16 September 2016, Pages 716-720
Journal: Biochemical and Biophysical Research Communications - Volume 478, Issue 2, 16 September 2016, Pages 716-720
نویسندگان
Mina Thon, Toru Hosoi, Koichiro Ozawa,