کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2583397 1130690 2014 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
The protective role of ferulic acid on sepsis-induced oxidative damage in Wistar albino rats
ترجمه فارسی عنوان
نقش محافظ فرولیک اسید در آسیب اکسیداتیو ناشی از سپسیس در سر موش نر نژاد ویستار
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی


• The effects of ferulic acid (FA) on sepsis-induced oxidative damage in thelymphocytes, liver and kidney cells of Wistar albino rats were investigated.
• The DNA damage was found to be significantly higher in the sepsis-induced rats (p < 0.05).
• The Comet parameters were significantly decreased in the FA-treated sepsis-induced group when compared with the sepsis-induced group.
• FA treatment also decreased the malondialdehyde (MDA) levels and glutathione peroxidase (GSH-Px) activities and increased the glutathione (GSH) levels and superoxide dismutase (SOD) activities in the sepsis-induced rats.

Oxidative stress has an important role in the development of sepsis-induced multiorgan failure. Ferulic acid (FA), a well-established natural antioxidant, has several pharmacological activities including anti-inflammatory, anticancer and hepatoprotective. This study aimed to investigate the effects of FA on sepsis-induced oxidative damage in Wistar albino rats. Sepsis-induced DNA damage in the lymphocytes, liver and kidney cells of rats were evaluated by comet assay with and without formamidopyrimidine DNA glycosylase (Fpg). The oxidative stress parameters such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and total glutathione (GSH) and malondialdehyde (MDA) levels were also measured. It is found that DNA damage in sepsis + FA-treated group was significantly lower than the sepsis group. FA treatment also decreased the MDA levels and increased the GSH levels and SOD and GSH-Px activities in the sepsis-induced rats. It seems that FA might have ameliorative effects against sepsis-induced oxidative damage.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Environmental Toxicology and Pharmacology - Volume 38, Issue 3, November 2014, Pages 774–782
نویسندگان
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