| Objective To investigate the effects of Simvastatin on the expressions of Axin and β-catenin in rat kidney tissue treated with ischemia-reperfusion.Methods Thirty-six male Wistar rats were randomly divided into3groups (n=6each): sham operation group (group Sham), ischemia-reperfusion group (group IR), Simvastatin group (group XF). Rats treated with IR injury were killed after6hour or48hour and the contents of serum creatinine (Scr) were detected respectively. The pathological results in the kidney tissue of these rats were also observed by optical microscope. Besides, the expression of Axin and β-catenin were detected by FQ-PCR and immunohistochemistry.Results After the rats in the group IR treated with ischemia-reperfusion for6or48h, it was found that the levels of Scr value in the group IR were higher (P<0.05) than those of group Sham, meanwhile the levels of Scr value in the case of48h treatment was higher than those of6h treatment in the froup IR. In the sham group, the organizational structure of renal were normal. In the group IR, the renal tubular epithelial cells had different degree swelling, necrosis, fall off and inflammatory cells infiltrating obviously in renal interstitial. But in the group XF, the renal injury induced by IR in rats could be attenuated distinctly after addition of simvastatin. The levels of Axin protein content and mRNA expression in rat kidney tissue were significantly decreased (P<0.05), meanwhile, the levels of β-catenin protein content and mRNA expression in the group IR were significantly increased compared with group Sham (P<0.05). In the group XF, the levels of Axin protein and mRNA content were significantly decreased compared with group IR (P<0.05), and the levels of β-catenin protein content and mRNA expression were significantly increased compared with group IR (P<0.05). In addition, the expressions of Axin was inversely correlated with the content of β-catenin (P<0.05).Conclusion Simvastatin could significantly alleviate renal tissue damages induced by IR injury. It was possibly attributed to the restraining effect of Simvastatin on the expression of Axin, which facilitated the accumulation of β-catenin in the cell nucleus and activated the downstream of target genes. |