Attenuation of reperfusion injury by renal ischemic postconditioning: The role of NO

作者：Liu Xiuheng^*; Chen Hui; Zhan Bingyan; Xing Bianzhi; Zhou Jiangqiao; Zhu Hengcheng; Chen Zhiyuan

来源：Biochemical and Biophysical Research Communications, 2007, 359(3): 628-634.

DOI：10.1016/j.bbrc.2007.05.129

• ischemic postconditioning
• kidney
• ischemia
• NO
• eNOS
• iNOS
• ET-1

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.

• 出版日期2007-8-3
• 单位华中科技大学; 武汉大学