Effects of Fufang Shenhua Tablet(复方肾华片) on the Expression of Toll-Like Receptors during Acute Kidney Injury Induced by Ischemia-Reperfusion in Rats

<正>Objective:To investigate the impact of a traditional Chinese medicinal compound known as Fufang Shenhua Tablet(复方肾华片,SHP) on the expression of Toll-like receptors(TLRs) during renal ischemia-reperfusion injury(IRI)-induced acute kidney injury(AKI) in rats.Methods:A total of 28 Wistar rats were randomly divided into five groups:(1) pseudo-operation control group,(2) ischemia-reperfusion model group, (3) Astragaloside group,(4) high-dose SHP group,and(5) low-dose SHP group.There were four rats in the pseudo-operation group and six rats in each of the other groups.The accepted ischemia-reperfusion model was established after a 7-day gavage intervention,and pathological changes and renal function were observed,using an enzyme-linked immunosorbent assay(ELISA) to detect interleukin 8(IL-8) and interferon gamma(IFN-γ) levels,as well as immunohistochemical staining to detect altered levels of TLR2 and TLR4 expression in renal tissue.Results:After 24 h,renal pathological damage and the expression levels of serum creatinine(Scr),IL-8, IFN-γ,TLR2,and TLR4 were significantly higher in the model group as compared with the pseudo-operation group(P0.05).In addition,at 24 h the above indicators decreased significantly in the Astragaloside group,high-dose SHP group and low-dose SHP group as compared with the ischemia-reperfusion model group(P0.05). TLR2 and TLR4 expression levels were significantly reduced in the SHP treatment and Astragaloside group as compared with the pseudo-operation group(P0.05).Further,the high-dose SHP group showed significantly less renal damage score and decreased levels of TLR expression than those of low-dose SHP group and Astragaloside group(all P0.05).Conclusion:SHP can alleviate the renal structural and functional damage caused by IRI-induced AKI in rats by reducing the damage of renal pathology,which may reduce inflammatory cytokine levels by downregulating the expression of TLRs in renal tissue in a dose-dependent manner.