کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
8547815 1561733 2018 32 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Diet with high content of advanced glycation end products induces systemic inflammation and weight gain in experimental mice: Protective role of curcumin and gallic acid
ترجمه فارسی عنوان
رژیم غذایی با محتوای بالایی از محصولات نهایی پیشرفته گلیساسیون باعث التهاب سیستمیک و افزایش وزن در موش های آزمایشی می شود: نقش محافظتی کورکومین و اسید گالیک
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک دانش تغذیه
چکیده انگلیسی
The present study was aimed to investigate the effect of diet derived AGEs (dAGEs) on the circulatory levels of pro-inflammatory cytokines, chemokines and to evaluate the protective efficacy of natural anti-oxidants curcumin (CU) and gallic acid (GA) respectively against the dAGEs-induced systemic inflammation in experimental Swiss albino mice. The experimental mice were fed with dAGEs in the presence and absence of CU and GA for 6 months. The levels of 40 circulatory pro-inflammatory cytokines and chemokines were evaluated using Proteome-Cytokine Array kit. In addition, serum levels of N-ɛCML, CRP and HbA1c were estimated by ELISA method. Among the sixteen pro- and anti-inflammatory cytokines analysed, five (IL-16, IL-1α, ICAM, TIMP-1 and C5a) were found to be highly expressed (3.5-fold) and eleven cytokines were moderately expressed (2-fold) in dAGEs fed mice. In case of chemokines, three (BLC, SDF-1 and MCP-1) were found to be highly expressed (4-fold) and ten showed moderate expression (2-fold) as compared with basal diet fed mice. Interestingly, CU or GA co-treatment normalized the levels of circulatory pro- and anti-inflammatory cytokines, chemokines, N-ɛCML, CRP and HbA1c levels. Together, the present study suggests that dAGEs are positively associated with the development of systemic inflammation in experimental mice.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Food and Chemical Toxicology - Volume 114, April 2018, Pages 237-245
نویسندگان
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