Tripterysium glycosides preconditioning attenuates renal ischemia/reperfusion injury in a rat model.

Autor: Wang, Zhi-shun, Qiu, Tao, Liu, Xiu-heng, Zhou, Jiang-qiao, Chen, Zhong-bao, Wang, Lei, Zhang, Long, Shen, Ye, Zhang, Lu
Zdroj: International Urology & Nephrology; Feb2016, Vol. 48 Issue 2, p213-221, 9p
Abstrakt: Background: Ischemia-reperfusion (I/R) injury to the kidney occurs commonly in organ transplantation from donation after cardiac death, involving many pathologic processes. In this study, we used rat model to assess whether tripterysium glycosides (TG) preconditioning could exert protective effects in renal I/R injury. Materials and methods: All male SD rats were randomly divided into four groups (6 each): sham group, TG group, I/R group and TG + I/R group. Groups TG and TG + I/R were pretreated with TG at 0.1 mg/kg for 14 days; groups sham and I/R were administered with the same dosage of normal saline. Groups TG + I/R and I/R underwent 45 min of renal ischemia of left kidney after right nephrectomy, and then, they were subjected to 72-h reperfusion. Groups sham and TG were only received right nephrectomy. The indicators of apoptosis, fibrosis and inflammation were analyzed to evaluate the effect of tripterysium glycosides preconditioning on renal I/R injury. Results: Pretreatment with TG significantly inhibited the levels of serum creatine and blood urea nitrogen and improved histologic lesions induced by I/R injury. Moreover, for the apoptosis signal pathway, pretreatment with TG markedly decreased the expression of caspase-3 and Bax and increased the level of Bcl-2. HMGB1, which was regarded as one of inflammation marker molecule, it was inhibited in the TG + I/R group. For the fibrosis signal pathway, the pretreatment with TG before I/R could down-regulate the expression level of typical molecules of fibrosis (TGF-β1, Smad3, p-Smad3). Conclusions: Pretreatment with tripterysium glycosides exhibited protective effect on kidney ischemia/reperfusion injury, which might be related to the alleviation of inflammation, fibrosis and the reduction in apoptosis. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index