Effect of nifedipine on renal ischemia-reperfusion injury in rats
10.3760/cma.j.issn.0254-1416.2010.11.029
- VernacularTitle:硝苯地平对大鼠肾缺血再灌注损伤的影响
- Author:
Yan LIU
;
Xiaohong XIA
;
Zhihui MIAO
;
Yanling WANG
;
Lihua HONG
- Publication Type:Journal Article
- Keywords:
Nifedipine;
Kidney;
Reperfusion injury
- From:
Chinese Journal of Anesthesiology
2010;30(11):1378-1380
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of nifedipine on renal ischemia-reperfusion injury (I/R) in rats and the possible mechanism. Methods Forty-two male SD rats weighing 220-250 g were randomly divided into 3 groups with 14 animals in each group: sham operation group (group S); I/R group and I/R + nifedipine group (group N). The renal ischemia was induced by occlusion of bilateral renal arteries and veins for 45 min followed by reperfusion. In group S the renal arteries and veins were only exposed but not occluded. In group N, nifedipine 0.1 mg/kg was injected via the tail vein 15 min before ischemia and 15 min before reperfusion, while the equal volume of solvent was given in group I/R. The urine was collected to detect the N-acetyl-β-D-glucosaminide (NAG) activities at 6 and 24 h of reperfusion. Arterial blood samples were taken at 6 and 24 h reperfusion for determination of concentrations of serum creatinine (Cr), malondialdehyde (MDA) and NO. The rats were then sacrificed and the kidney was removed to detect the apoptotic cells in renal cortex and expression of heat shock protein 70 (HSP70) and endothelin- 1 (ET-1). Results The concentrations of serum Cr and MDA, NAG activity, expression of HSP70 and ET-1 and apoptosis rate were significantly increased in group I/R compared with group S (P ＜0.05). The concentrations of serum Cr and MDA, NAG activity, ET-1 expression and apoptosis rate were significantly decreased, while the serum NO concentration was significantly increased in group N compared with group I/R (P ＜ 0.05). Conclusion Nifedipine can attenuate renal I/R injury and the underlying mechanism may be related to the inhibition of ET-1 expression.
