کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5549374 1402870 2016 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Protodioscin ameliorates fructose-induced renal injury via inhibition of the mitogen activated protein kinase pathway
ترجمه فارسی عنوان
پروتودیوسین باعث کاهش آسیب کلیه ناشی از فروکتوز به دلیل مهار پروتئین کیناز فعال میتوکند
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیوشیمی بالینی
چکیده انگلیسی

BackgroundHigh dietary fructose can cause metabolic syndrome and renal injury.PurposeThe effects of protodioscin on metabolic syndrome and renal injury were investigated in mice receiving high-dose fructose.MethodsMice received 30% (w/v) fructose in water and standard chow for 6 weeks to induce metabolic syndrome and were divided into four groups to receive carboxymethylcellulose sodium, allopurinol (5 mg/kg) and protodioscin (5 and 10 mg/kg) continuously for 6 weeks, respectively. The glucose intolerance, serum uric acid (UA), blood urea nitrogen (BUN), creatinine (Cr), total cholesterol (TC), triglyceride (TG), interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were determined.ResultsProtodioscin significantly improved glucose intolerance and reduced the levels of serum UA, BUN, Cr, TC and TG. Histological examinations showed that protodioscin ameliorated glomerular and tubular pathological changes. Protodioscin significantly reduced renal concentrations of IL-1β, IL-6 and TNF-α by inhibiting the activation of nuclear factor-κB, c-Jun N-terminal kinase, p38 mitogen-activated protein kinase and extracellular signal-regulated kinase. In addition, the effect of protodioscin on the mitogen activated protein kinases (MAPK) pathway was examined.ConclusionTaken together, protodioscin is a potential drug candidate for high dietary fructose-induced metabolic syndrome and renal injury.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Phytomedicine - Volume 23, Issue 12, 15 November 2016, Pages 1504-1510
نویسندگان
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