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Autophagy activation attenuates renal ischemia-reperfusion injury in rats
Zhang, Ya-Li; Zhang, Jie; Cui, Li-Yan; Yang, Shuo
关键词Autophagy Ischemia Reperfusion Apoptosis Acute Kidney Injury
刊名EXPERIMENTAL BIOLOGY AND MEDICINE
2015-12-01
DOI10.1177/1535370215581306
240期:12页:1590-1598
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Medicine, Research & Experimental
研究领域[WOS]Research & Experimental Medicine
关键词[WOS]ACUTE KIDNEY INJURY ; TUBULAR APOPTOSIS ; CELL-DEATH ; FAILURE ; ISCHEMIA/REPERFUSION ; MECHANISMS ; PROTECTS ; INHIBITION ; CASPASE-3 ; RAPAMYCIN
英文摘要

Ischemia-reperfusion (I/R) injury is a leading cause of acute kidney injury (AKI), which is a common clinical complication but lacks effective therapies. This study investigated the role of autophagy in renal I/R injury and explored potential mechanisms in an established rat renal I/R injury model. Forty male Wistar rats were randomly divided into four groups: Sham, I/R, I/R pretreated with 3-methyladenine (3-MA, autophagy inhibitor), or I/R pretreated with rapamycin (autophagy activator). All rats were subjected to clamping of the left renal pedicle for 45min after right nephrectomy, followed by 24h of reperfusion. The Sham group underwent the surgical procedure without ischemia. 3-MA and rapamycin were injected 15min before ischemia. Renal function was indicated by blood urea nitrogen and serum creatinine. Tissue samples from the kidneys were scored histopathologically. Autophagy was indicated by light chain 3 (LC3), Beclin-1, and p62 levels and the number of autophagic vacuoles. Apoptosis was evaluated by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method and expression of caspase-3. Autophagy was activated after renal I/R injury. Inhibition of autophagy by 3-MA before I/R aggravated renal injury, with worsened renal function, higher renal tissue injury scores, and more tubular apoptosis. In contrast, rapamycin pretreatment ameliorated renal injury, with improved renal function, lower renal tissue injury scores, and inhibited apoptosis based on fewer TUNEL-positive cells and lower caspase-3 expression. Our results demonstrate that autophagy could be activated during I/R injury and play a protective role in renal I/R injury. The mechanisms were involved in the regulation of several autophagy and apoptosis-related genes. Furthermore, autophagy activator may be a promising therapy for I/R injury and AKI in the future.

语种英语
WOS记录号WOS:000366000500005
项目编号81271903 ; 2012BA137B01
资助机构Natural Science Foundation of China ; National Science and Technology Ministry
引用统计
被引频次:10[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/55627
专题北京大学第三临床医学院
北京大学医学部管理机构_医学部
北京大学第三临床医学院_检验科
作者单位Peking Univ, Dept Lab Med, Hosp 3, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Zhang, Ya-Li,Zhang, Jie,Cui, Li-Yan,et al. Autophagy activation attenuates renal ischemia-reperfusion injury in rats[J]. EXPERIMENTAL BIOLOGY AND MEDICINE,2015,240(12):1590-1598.
APA Zhang, Ya-Li,Zhang, Jie,Cui, Li-Yan,&Yang, Shuo.(2015).Autophagy activation attenuates renal ischemia-reperfusion injury in rats.EXPERIMENTAL BIOLOGY AND MEDICINE,240(12),1590-1598.
MLA Zhang, Ya-Li,et al."Autophagy activation attenuates renal ischemia-reperfusion injury in rats".EXPERIMENTAL BIOLOGY AND MEDICINE 240.12(2015):1590-1598.
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