کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2804491 1156876 2009 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
The effect of 1α,25(OH)2D3 vitamin over oxidative stress and biochemical parameters in rats where Type 1 diabetes is formed by streptozotocin
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی علوم غدد
پیش نمایش صفحه اول مقاله
The effect of 1α,25(OH)2D3 vitamin over oxidative stress and biochemical parameters in rats where Type 1 diabetes is formed by streptozotocin
چکیده انگلیسی

IntroductionThe 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3] plays an essential role in mineral balance but has also been recognized as a powerful modulator of immune response. We aimed to examine the effect of the 1α,25(OH)2D3 treatment on insulin/c-peptide, catalase, superoxide dismutase (SOD), and blood glucose in rats that take streptozotocin (STZ).MethodsForty pieces of male rats of Albino family whose average weights were 261.00±07.62 g were used in the study. Rats were made diabetic by giving STZ of 40 mg/kg during 5 days through intraperitoneal path. Some of the diabetic group and nondiabetic group were received 1α,25(OH)2D3. The levels of SOD, insulin, c-peptide, glucose, SOD, and catalase were measured at the zero, second, fourth, and sixth weeks.ResultsErythrocyte SOD levels didn't show a significant difference at the end of the sixth week in all groups when compared to the beginning. While erythrocyte catalase levels didn't show a significant difference in nondiabetic control and nondiabetic with vitamin D, and diabetic with vitamin D groups at the end of sixth week when compared to the beginning, a significant measurement was made in diabetic without vitamin D group. Maximal insulinitis scoring values were observed in diabetic without vitamin D that didn't receive 1α,25(OH)2D3 treatment.ConclusionThe highness of insulin and c-peptide levels in the group that received treatment when compared to other groups and the lowness of oxidative markers such as SOD, catalase in this study can be explained by the fact that 1α,25(OH)2D3 treatment prevents the intervention of apoptosis mechanism.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Diabetes and its Complications - Volume 23, Issue 6, November–December 2009, Pages 401–408
نویسندگان
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