کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2022432 | 1542396 | 2014 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Protective effect of short-term treatment with parathyroid hormone 1-34 on oxidative stress is involved in insulin-like growth factor-I and nuclear factor erythroid 2-related factor 2 in rat bone marrow derived mesenchymal stem cells
ترجمه فارسی عنوان
اثر حفاظتی درمان کوتاه مدت با هورمون پاراتیروئید 1-34 بر استرس اکسیداتیو درگیر در فاکتور 2 مرتبط با فاکتور رشد شبه انسولین و اریتروئید فاکتور هسته ای 2 در مشتق از مغز استخوان سلول های بنیادی مزانشیمی استخوان رت است
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کلمات کلیدی
MSCiNOSIGF-IpTHNRF-2ROS - ROSOxidative stress - تنش اکسیداتیوMesenchymal stem cells - سلول های بنیادی مزانشیمیinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییInsulin-like growth factor-I - عامل رشد انسولین مانند Inuclear factor erythroid 2-related factor 2 - فاکتور هسته ای عامل erythroid 2 مرتبط 2heme oxygenase - همگام اکسژنازparathyroid hormone - هورمون پاراتیروئیدReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
چکیده انگلیسی
Bone marrow-derived mesenchymal stem cell (MSC)-mediated regeneration is a promising treatment for degenerative disease and traumatic injuries. MSCs can be isolated from rats using magnetic-activated cell sorting with CD105 antibody. We investigated the relationships between the expression of endogenous insulin-like growth factor-I (IGF-I) and nuclear factor erythroid 2-related factor 2 (Nrf-2) during short-term treatment with parathyroid hormone (PTH) 1-34-induced protective response in MSCs. PTH 1-34 (10â 9 M) decreased reactive oxygen species (ROS) generation but increased cell viability and endogenous IGF-I (p < 0.01). Suppression of IGF-I and Nrf-2 using specific small interfering RNA (siRNA) blocked the effects of PTH 1-34. Furthermore, increasing cell viability of PTH against hydrogen peroxide (H2O2) was suppressed by treatment with siRNA to IGF-I and Nr-2 (p < 0.05). Exogenous IGF-I (10â 9 M) also increased endogenous IGF-I, cell viability, and Nrf-2 expression. These incremental increases were lessened by Nrf-2 siRNA (p < 0.05). Exogenous IGF-I also inhibited the increase of H2O2-induced ROS generation, and the decrease of PTH 1-34-induced ROS generation in the presence of IGF-I and Nrf-2 siRNA. The increase of PTH 1-34-induced Nrf-2 expression was more significant in the nucleus than in the cytosol (p < 0.05). PTH 1-34 also inhibited H2O2-induced inducible nitric oxide synthase expression, but increased the expression of heme oxygenase 1/2. The results implicate PTH 1-34, Nrf-2, and IGF-I signaling pathways in the response to oxidative stress. These factors could influence IGF-I regulation of metabolic fate and survival in MSCs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Regulatory Peptides - Volume 189, 10 February 2014, Pages 1-10
Journal: Regulatory Peptides - Volume 189, 10 February 2014, Pages 1-10
نویسندگان
Young-Il Oh, Jong-Hoon Kim, Chang-Won Kang,