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

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-Dawl...

Full description

Bibliographic Details
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:
Online Access:http://dx.doi.org/10.1080/0886022X.2018.1497517
_version_ 1818408711824080896
author Xiao Wang
Wei Wang
Jian-Zhong Wang
Cheng Yang
Chao-Zhao Liang
author_facet Xiao Wang
Wei Wang
Jian-Zhong Wang
Cheng Yang
Chao-Zhao Liang
author_sort Xiao Wang
collection DOAJ
description 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.
first_indexed 2024-12-14T09:48:05Z
format Article
id doaj.art-58579b420c884e1f98c37c790ae82bfe
institution Directory Open Access Journal
issn 0886-022X
1525-6049
language English
last_indexed 2024-12-14T09:48:05Z
publishDate 2018-10-01
publisher Taylor & Francis Group
record_format Article
series Renal Failure
spelling doaj.art-58579b420c884e1f98c37c790ae82bfe2022-12-21T23:07:35ZengTaylor & Francis GroupRenal Failure0886-022X1525-60492018-10-0140149850510.1080/0886022X.2018.14975171497517Effect of apigenin on apoptosis induced by renal ischemia/reperfusion injury in vivo and in vitroXiao Wang0Wei Wang1Jian-Zhong Wang2Cheng Yang3Chao-Zhao Liang4The First Affiliated Hospital of Anhui Medical UniversityThe First Affiliated Hospital of Anhui Medical UniversityThe First Affiliated Hospital of Anhui Medical UniversityThe First Affiliated Hospital of Anhui Medical UniversityThe First Affiliated Hospital of Anhui Medical UniversityObjectives: 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.http://dx.doi.org/10.1080/0886022X.2018.1497517Apigeninrenal ischemia/reperfusion (I/R) injuryapoptosisBcl-2AKt
spellingShingle Xiao Wang
Wei Wang
Jian-Zhong Wang
Cheng Yang
Chao-Zhao Liang
Effect of apigenin on apoptosis induced by renal ischemia/reperfusion injury in vivo and in vitro
Renal Failure
Apigenin
renal ischemia/reperfusion (I/R) injury
apoptosis
Bcl-2
AKt
title Effect of apigenin on apoptosis induced by renal ischemia/reperfusion injury in vivo and in vitro
title_full Effect of apigenin on apoptosis induced by renal ischemia/reperfusion injury in vivo and in vitro
title_fullStr Effect of apigenin on apoptosis induced by renal ischemia/reperfusion injury in vivo and in vitro
title_full_unstemmed Effect of apigenin on apoptosis induced by renal ischemia/reperfusion injury in vivo and in vitro
title_short Effect of apigenin on apoptosis induced by renal ischemia/reperfusion injury in vivo and in vitro
title_sort effect of apigenin on apoptosis induced by renal ischemia reperfusion injury in vivo and in vitro
topic Apigenin
renal ischemia/reperfusion (I/R) injury
apoptosis
Bcl-2
AKt
url http://dx.doi.org/10.1080/0886022X.2018.1497517
work_keys_str_mv AT xiaowang effectofapigeninonapoptosisinducedbyrenalischemiareperfusioninjuryinvivoandinvitro
AT weiwang effectofapigeninonapoptosisinducedbyrenalischemiareperfusioninjuryinvivoandinvitro
AT jianzhongwang effectofapigeninonapoptosisinducedbyrenalischemiareperfusioninjuryinvivoandinvitro
AT chengyang effectofapigeninonapoptosisinducedbyrenalischemiareperfusioninjuryinvivoandinvitro
AT chaozhaoliang effectofapigeninonapoptosisinducedbyrenalischemiareperfusioninjuryinvivoandinvitro