کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5551003 1557716 2017 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
The impact of gallic acid on the methotrexate-induced kidney damage in rats
ترجمه فارسی عنوان
تأثیر اسید گالیکیک بر آسیب کلیه ناشی از متوترکسات در موش صحرایی
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک دانش تغذیه
چکیده انگلیسی


- Methotrexate (MTX) increased blood urea nitrogen, creatinine, uric acid levels and tissue oxidative stress markers.
- Gallic acid ameliorated MTX induced pathologies.
- Serum Amyloid A, tumor necrosis alpha, protoglandin E2 and C-reactive protein in tubuler epithelium increased by MTX.

Prolonged use of an antineoplastic agent methotrexate (MTX), can cause numerous side effects such as nephrotoxicity. The aim of this study was to examine the effects of MTX on kidneys and demonstrate the protective effects of gallic acid (GA). Twenty-four, male, rats distributed into three groups. Each groups consisted eight rats and only saline was administered to the control group. The MTX group received a single dose (20 mg/kg) MTX intraperitoneally. The MTX + GA group received same dose MTX and 100 mg/kg GA orally during the 7 days. Renal functions, oxidative stress markers, histopathological and immunohistochemical changes were evaluated at the end of the experiment. Blood urea nitrogen, creatinine, uric acid levels and tissue oxidative stress markers, total oxidant status and oxidative stress index levels significantly increased and total antioxidant status levels significantly decreased in MTX group compared with the control group. At the histopathological examination hemorrhages, tubular cell necrosis, glomerulosclerosis, inflammatory cell infiltrations and proteinous materials in tubules were noticed in MTX group. Immunohistochemical examination revealed that increased expressions of serum amyloid A (SAA), tumor necrosis factor alpha (TNF-α), prostaglandin E2 (PGE-2) and C-reactive protein (CRP) in tubular epithelial cells of kidneys in this group. There were no immunoreaction with SAA and CRP, only small number of PGE-2 and TNF-α positive tubular epithelial cells were observed in MTX + GA group. In conclusion, all evidence suggested that oxidative stress caused MTX-induced nephrotoxicity and GA prevent the kidney from the nephrotoxicity due to its antioxidant and anti-inflammatory activities.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Food and Drug Analysis - Volume 25, Issue 4, October 2017, Pages 890-897
نویسندگان
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