کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10767272 | 1050718 | 2007 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Attenuation of reperfusion injury by renal ischemic postconditioning: The role of NO
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
Ischemic postconditioning (Postcond) is defined as rapid intermittent interruptions of blood flow in the early phase of reperfusion and mechanically alters the hydrodynamics of reperfusion. Although Postcond has been demonstrated to attenuate ischemia/reperfusion (I/R) injury in the heart and brain, its roles to renal I/R injury remain to be defined. In the present study, we examined the role of Postcond in I/R injury in a right-nephrectomized rat model. Postcond prevents the renal dysfunction and cell apoptosis induced by I/R and increases nitric oxide (NO) release and renal NO synthase (endothelial, eNOS and inducible, iNOS) expression. In contrast, enhancement of endothelin-1 (ET-1) in the kidney after the reperfusion was markedly suppressed by Postcond. These findings indicate that Postcond can inhibit renal I/R injury. The protective effect of Postcond is closely related to the NO production following the increase in eNOS and iNOS expression and the suppressive effect of ET-1 overproduction.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 359, Issue 3, 3 August 2007, Pages 628-634
Journal: Biochemical and Biophysical Research Communications - Volume 359, Issue 3, 3 August 2007, Pages 628-634
نویسندگان
Xiuheng Liu, Hui Chen, Bingyan Zhan, Bianzhi Xing, Jiangqiao Zhou, Hengcheng Zhu, Zhiyuan Chen,