کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8337217 | 1540659 | 2014 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Increase in AMPK brought about by cocoa is renoprotective in experimental diabetes mellitus by reducing NOX4/TGFβ-1 signaling
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کلمات کلیدی
AMPKExtracellular matrix accumulationTGFβ-1H2DCF-DADiabetic nephropathy (DN)PAI-1PKCdichlorofluoresceinDCF-DASTZEPIepicatechinNADPHECMAICAR5-aminoimidazole-4-carboxamide ribonucleotideLASAER - AIRMTT - MTTSmall interfering RNA - RNA تداخل کوچکROS - ROSsiRNA - siRNAstreptozotocin - استرپتوزوتوسینperiodic acid-Schiff - اسید فسفریک Schifftransforming growth factor β-1 - تبدیل فاکتور رشد β-1compound C - ترکیب CSpontaneously Hypertensive Rat - خودآزمایی موش بالینیdichlorodihydrofluorescein diacetate - دی کلستیدوفروفوروزین دی سکتهDiabetes mellitus - دیابت قندیShr - شریPlasminogen activator inhibitor-1 - مهار کننده فعال کننده پلاسمینوژن-1Albumin excretion rate - میزان دفع آلبومینDiabetic nephropathy - نفروپاتی دیابتیPAS - نهnicotinamide adenine dinucleotide phosphate - نیکوتین آمید adenine dinucleotide phosphateProtein kinase C - پروتئین کیناز سی5′ adenosine monophosphate-activated protein kinase - پروتئین کیناز فعال شده با آدنوزین مونوفسفات 5 'HPLC - کروماتوگرافی مایعی کاراhigh-performance liquid chromatography - کروماتوگرافی مایعی کاراhigh glucose - گلوکز بالا یا قند بالاnormal glucose - گلوکز طبیعیReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The aims of the present study were to investigate, in diabetes mellitus (DM), the mechanism of NOX4 up-regulation, its link with 5â² adenosine monophosphate-activated protein kinase (AMPK) inactivation and transforming growth factor (TGF) Ã-1 signaling in determining the accumulation of kidney extracellular matrix (ECM), and the possible action of cocoa enriched with polyphenols (CH) in these events. After 16 weeks of DM, spontaneously hypertensive rats showed increased kidney TGFβ-1 levels and expression of phosphorylated smad2, collagen IV and fibronectin in parallel with elevated NOX4 expression and reduced phosphorylated AMPK. CH treatment in diabetic rats prevented all of these abnormalities. In immortalized human mesangial cells exposed to high glucose (HG), or TGFβ-1, CH, nicotinamide adenine dinucleotide phosphate blocker, or silencing NOX4 ameliorated enhanced phosphorylated smad2 and collagen IV. Reduction in phosphorylated AMPK induced by HG or TGFβ-1 was ameliorated by CH or activation of AMPK, which reduced phosphorylation of smad2 and collagen IV via reduction in NOX4 expression. The effects of CH were abolished by AMPK blockade. These results suggest that inactivation in AMPK leads to NOX4 up-regulation, activation of TGFβ-1 signaling and increased ECM accumulation. Additionally, increased TGF-Ã1 per se leads to the amplification of ECM production by reducing AMPK and promoting the activation of NOX4. It is suggested that the activation of AMPK by CH followed by reduction in NOX4/TGFβ-1 signaling may have a therapeutic potential in diabetic nephropathy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Nutritional Biochemistry - Volume 25, Issue 7, July 2014, Pages 773-784
Journal: The Journal of Nutritional Biochemistry - Volume 25, Issue 7, July 2014, Pages 773-784
نویسندگان
Alexandros Papadimitriou, Elisa B.M.I. Peixoto, Kamila C. Silva, Jacqueline M. Lopes de Faria, José B. Lopes de Faria,