کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8336974 | 1540649 | 2015 | 63 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
All-trans retinoic acid prevents oxidative stress-induced loss of renal tight junction proteins in type-1 diabetic model
ترجمه فارسی عنوان
اسید کلرید رتینوئیک مانع از دست دادن استرس اکسیداتیو پروتئین های اتصال کافی کلیه در مدل دیابت نوع 1
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کلمات کلیدی
دیابت، اتصالات تنگی کلیه، استرس اکسیداتیو، اسید رتینوئیک تمام ترانس، کلودینس،
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
چکیده انگلیسی
We previously reported that diabetes decreased the expression of renal tight junction (TJ) proteins claudin-5 in glomerulus, and claudin-2 and occludin in proximal tubule through an oxidative stress dependent way. Now we investigated whether all-trans retinoic acid (atRA), a compound that plays a relevant role in kidney maintenance and that possesses antioxidant properties, prevents loss of TJ proteins in streptozotocin (STZ)-treated rats. atRA was administered daily by gavage (1Â mg/kg) from Days 3-21 after STZ administration. atRA attenuated loss of body weight, proteinuria and natriuresis but it did not prevent hyperglucemia. Other metabolic alterations, such as: increased kidney injury molecule (KIM)-1, oxidative stress, protein kinase C (PKC) beta 2, NADPH oxidase subunits (p47phox and gp91phox) expressions and endothelial nitric oxide synthase (eNOS) uncoupling, and decreased nitric oxide synthesis, nuclear factor-erythroid-2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expressions were also attenuated by atRA. In vitro scavenging capacity assays showed that atRA scavenged peroxyl radicals (ROO
- ), singlet oxygen (1O2) and hypochlorous acid (HOCl) in a concentration-dependent manner. Decreased expressions of occludin, claudins-2 and -5 induced by diabetes were ameliorated by atRA. We also found that diabetes induced tyrosine nitration (3-NT), SUMOylation and phosphorylation in serine residues of claudin-2 and atRA prevented these changes. In conclusion, atRA exerted nephroprotective effects by attenuating oxidative stress and preventing loss of renal TJ proteins.
- ), singlet oxygen (1O2) and hypochlorous acid (HOCl) in a concentration-dependent manner. Decreased expressions of occludin, claudins-2 and -5 induced by diabetes were ameliorated by atRA. We also found that diabetes induced tyrosine nitration (3-NT), SUMOylation and phosphorylation in serine residues of claudin-2 and atRA prevented these changes. In conclusion, atRA exerted nephroprotective effects by attenuating oxidative stress and preventing loss of renal TJ proteins.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Nutritional Biochemistry - Volume 26, Issue 5, May 2015, Pages 441-454
Journal: The Journal of Nutritional Biochemistry - Volume 26, Issue 5, May 2015, Pages 441-454
نویسندگان
Eduardo Molina-Jijón, Rafael RodrÃguez-Muñoz, MarÃa del Carmen Namorado, Pablo Bautista-GarcÃa, Omar Noel Medina-Campos, José Pedraza-Chaverri, José L. Reyes,