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

• Main Authors: Xiao Wang, Wei Wang, Jian-Zhong Wang, Cheng Yang, Chao-Zhao Liang
• Format: Article
• Language: English
• Published: Taylor & Francis Group 2018-10-01
• Series: Renal Failure
• Subjects: Apigenin; renal ischemia/reperfusion (I/R) injury; apoptosis; Bcl-2; AKt
• Online Access: http://dx.doi.org/10.1080/0886022X.2018.1497517
• ISSN: 0886-022X; 1525-6049

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.