کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10749806 | 1050294 | 2016 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Tyrosol, an olive oil polyphenol, inhibits ER stress-induced apoptosis in pancreatic β-cell through JNK signaling
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کلمات کلیدی
protein kinase-like endoplasmic reticulum kinaseNormal-fat dietβ-Cell failureXBP-1HFDT2DUPRATF6BiP - BIPC/EBP-homologous protein - C / EBP-homologous proteinIRE1α - IRE1aER stress - استرس استCHOP - تکه کردنTyrosol - تیروزولApoptosis - خزان یاختهایType 2 diabetes - دیابت نوع 2high-fat diet - رژیم غذایی با چربی بالاendoplasmic reticulum - شبکه آندوپلاسمی activating transcription factor 6 - فعال کردن عامل رونویسی 6Unfolded protein response - پاسخ پروتئین آشکارBinding immunoglobulin Protein - پروتئین ایمونوگلوبولین BindingPERK - پرک
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Dysfunction of pancreatic β-cell is a major determinant for the development of type 2 diabetes. Because of the stimulated insulin secretion in metabolic syndrome, endoplasmic reticulum (ER) stress plays a central mediator for β-cell failure. In this study, we investigated whether an antioxidant phenolic compound, tyrosol protects against β-cell dysfunction associated with ER stress. To address this issue, we exposed pancreatic β cells, NIT-1 to tunicamycin with tyrosol. We found tyrosol diminished tunicamycin-induced cell death in a dose-dependent manner. We also detected tyrosol decreased the expressions of apoptosis-related markers. Exposure to tunicamycin evoked UPR response and co-treatment of tyrosol led to reduction of ER stress. These effects of tyrosol were mediated by the phosphorylation of JNK. Moreover, we confirmed supplement of tyrosol ameliorated β-cell loss induced by high fat feeding. Taken together, our study provides a molecular basis for signaling transduction of protective effect of tyrosol against ER stress-induced β-cell death. Therefore, we suggest tyrosol could be a potential therapeutic candidate for amelioration of type 2 diabetes.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 469, Issue 3, 15 January 2016, Pages 748-752
Journal: Biochemical and Biophysical Research Communications - Volume 469, Issue 3, 15 January 2016, Pages 748-752
نویسندگان
Hyunjung Lee, Sung Won Im, Chang Hwa Jung, Young Jin Jang, Tae Youl Ha, Jiyun Ahn,