کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8268426 | 1534954 | 2015 | 25 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
NOD2 activation induces oxidative stress contributing to mitochondrial dysfunction and insulin resistance in skeletal muscle cells
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کلمات کلیدی
DPIMDPNODOCRmuramyl dipeptideTMBNACDCF-DAIRS-1PRR2′,7′-dichlorofluorescin diacetate - 2 '، 7'-dichlorofluorescin diacetate3,3′,5,5′-tetramethylbenzidine - 3،3 '، 5،5'-تترامیلیل بنزیدینN-acetylcysteine - N-استیل سیستئینROS - ROSinflammation - التهاب( توروم) insulin receptor substrate-1 - انسولین گیرنده زیربخش 1Innate immunity - ایمنی ذاتیdiphenyliodonium - دیفنیلیدونیمFree radicals - رادیکال آزادMitochondrial function - عملکرد میتوکندریInsulin resistance - مقاومت به انسولینOxygen consumption rates - میزان مصرف اکسیژنReactive oxygen species - گونههای فعال اکسیژنpattern recognition receptor - گیرنده شناسایی الگو
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
Nucleotide-binding oligomerization domain protein-2 (NOD2) activation in skeletal muscle cells has been associated with insulin resistance, but the underlying mechanisms are not yet clear. Here we demonstrate the implication of oxidative stress in the development of mitochondrial dysfunction and insulin resistance in response to NOD2 activation in skeletal muscle cells. Treatment with the selective NOD2 ligand muramyl dipeptide (MDP) increased mitochondrial reactive oxygen species (ROS) generation in L6 myotubes. MDP-induced ROS production was associated with increased levels of protein carbonyls and reduction in citrate synthase activity, cellular ATP level, and mitochondrial membrane potential, as well as altered expression of genes involved in mitochondrial function and metabolism. Antioxidant treatment attenuated MDP-induced ROS production and restored mitochondrial functions. In addition, the presence of antioxidant prevented NOD2-mediated activation of MAPK kinases and the inflammatory response. This was associated with reduced serine phosphorylation of insulin receptor substrate-1 (IRS-1) and improved insulin-stimulated tyrosine phosphorylation of IRS-1 and downstream activation of Akt phosphorylation. These data indicate that oxidative stress plays a role in NOD2 activation-induced inflammatory response and that MDP-induced oxidative stress correlates with impairment of mitochondrial functions and induction of insulin resistance in skeletal muscle cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 89, December 2015, Pages 158-169
Journal: Free Radical Biology and Medicine - Volume 89, December 2015, Pages 158-169
نویسندگان
Chandan K. Maurya, Deepti Arha, Amit K. Rai, Shashi Kant Kumar, Jyotsana Pandey, Deepa R. Avisetti, Shasi V. Kalivendi, Amira Klip, Akhilesh K. Tamrakar,