Abstract: AIM: To explore the effect of shenfu injection on renal ischemia/reperfusion injury in rats and to observe the expression of nuclear factor kappa B (NF-κB), tumour necrosis factor-α (TNF-α) and intercellular adhension molecule-1 (ICAM-1).METHODS: 36 SD rats were divided into three groups randomly.There were 12 rats in each group.Renal ischemia/reperfusion injury was induced by left renal pedicle occlusion for 45 minutes, followed by reperfusion with contralateral nephrectomy in rats.In shenfu pretreatment group, the rats were pretreated 1 hour before ischemia with shenfu injection.In ischemia/reperfusion group and control group, the animals were both pretreated with 0.9% natrill chloride, but in control group, the left renal pedicle was isolated, however, occlusion of the pedicle was not performed.The blood and kidney tissue were harvested after 2 hours of reperfusion.The serum creatinine (Cr) and blood urea nitrogen (BUN) values were measured with an automatic analyzer.Immunohistochemistry were used to evaluated the expression levels of NF-κB and ICAM-1, the concentration of tumor necrosis factor-α (TNF-α) in the kidney and plasma was determined by enzyme-linked immunoadsordent assay (ELISA).RESULTS: Compared with control group, BUN and Cr were gradually increased in ischemia/reperfusion group (P<0.01).The average OD values of NF-κB and ICAM-1 protein were significantly higher in ischemia/reperfusion group than those in shenfu pretreatment group (P<0.01) and control group (P<0.01).The levels of TNF-α in the kidney tissue and plasma were markedly increased after reperfusion.By contrast, the levels of TNF-α in shenfu pretreatment group were significiantly lower than those in ischemia/reperfusion group (P<0.05).CONCLUSION: The results show that SF has a protective effect against renal ischemia/reperfusion injury, which may through inhibiting the activity of NF-κB and the expression of ICAM-1 and TNF-α.

Key words: ischemia/reperfusioninjury, shenfuinjection, nuclearfactorkappaB, intercellularadhensionmolecule-1, tumornecrosisfactor-α