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

被引:24
作者
Wang, Xiao [1 ,2 ,3 ]
Wang, Wei [1 ,2 ]
Wang, Jian-Zhong [1 ]
Yang, Cheng [1 ]
Liang, Chao-Zhao [1 ,2 ]
机构
[1] Anhui Med Univ, Affiliated Hosp 1, Dept Urol, 238 Ji Xi Rd, Hefei 230022, Anhui, Peoples R China
[2] Anhui Med Univ, Inst Urol, Hefei, Anhui, Peoples R China
[3] Fuyang Peoples Hosp, Dept Urol, Fuyang, Peoples R China
基金
中国国家自然科学基金;
关键词
Apigenin; renal ischemia/reperfusion (I/R) injury; apoptosis; Bcl-2; AKt; ACUTE KIDNEY INJURY; ISCHEMIA-REPERFUSION INJURY; CELL-DEATH; PI3K/AKT; PROTECTS; BCL-2; INFLAMMATION; INVOLVEMENT; ACTIVATION; MODEL;
D O I
10.1080/0886022X.2018.1497517
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:498 / 505
页数:8
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