Effect of apigenin on apoptosis induced by renal ischemia/reperfusion injury in vivo and in vitro

Abstract

Objectives: This study aims to investigate the effects and molecular mechanisms of apigenin (ApI) on renal ischemia/reperfusion (I/R) injury in vivo and in vitro.

Methods: In vivo, the left renal artery was clamped for 45 min and the right kidney was removed to study renal I/R injury on Sprague-Dawley (SD) rats. ApI was injected at 60 min before renal ischemia. In vitro, renal tubular epithelial cells (HK-2) were pretreated with or without ApI (20 uM) for 60 min and then treated with hypoxia/reoxygenation (H/R). Renal function, histology, cells apoptosis, and cell viability were tested. Furthermore, the potential molecular mechanisms were assessed.

Results: ApI pretreatment could significantly alleviated the renal function and the pathological damage as well as cells apoptosis after I/R injury. Meanwhile, ApI treatment protects H/R induced HK-2 cell apoptosis in vitro. The results of Western blot showed that ApI significantly increased the expressions of B-cell lymphoma 2 (Bcl-2) and phosphor-AKt (p-AKt), Phosphoinositide 3-kinase (PI3K), while down-regulated the expressions of Caspase3 and Bax induced by H/R injury.

Conclusions: ApI pretreatment can protect renal function against I/R injury and prevent renal tubular cells from apoptosis in vivo and in vitro which might through PI3K/Akt mediated mitochondria-dependent apoptosis signaling pathway.

Keywords:

• Apigenin
• renal ischemia/reperfusion (I/R) injury
• apoptosis
• Bcl-2
• AKt

Disclosure statement

Authors declare no conflict of interest and the results presented in this article have not been published previously in whole or part, except in abstract format.

Additional information

Funding

This work was supported by a grant from the National Natural Science Foundation of China (Nos. 81401518 and 81370856) and Anhui Provincial Science Foundation [No. 1408085QH180].