促红细胞生成素受体激活通过激活ERK/p53信号通路保护肾脏免受缺血/再灌注诱导的细胞凋亡。
Erythropoietin Receptor Activation Protects the Kidney From Ischemia/Reperfusion-Induced Apoptosis by Activating ERK/p53 Signal Pathway.
作者信息
Zou Y-R, Zhang J, Wang J, Peng L, Li G-S, Wang L
机构信息
Department of Nephrology, Center of Electronic Science Technology and University of Electronic Science and Technology, Sichuan Academy of Sciences and Sichuan Provincial People's Hospital, Chengdu, People's Republic of China.
Department of General Medicine, Center of Electronic Science Technology and University of Electronic Science and Technology, Sichuan Academy of Sciences and Sichuan Provincial People's Hospital, Chengdu, People's Republic of China.
出版信息
Transplant Proc. 2016 Jan-Feb;48(1):217-21. doi: 10.1016/j.transproceed.2016.01.009.
BACKGROUND
Apoptosis plays an important role in renal ischemia/reperfusion (IR) injury. Evidence has shown that erythropoietin (EPO) has an antiapoptotic effect. Therefore, this study aimed to explore the effect and potential mechanism of EPO in renal IR injury.
METHODS
Kidney IR injury in rats was established by clamping the left renal artery for 30 minutes followed by 24 hours of reperfusion, along with contralateral nephrectomy. Renal function, renal histology, and expression of EPOR, p-EPOR, ERK, p-ERK, p-p53, p53, Bcl-2, Bcl-xl, Bad, and Bax were examined.
RESULTS
Pretreatment with EPO significantly reduced renal dysfunction, pathologic change, and expression of Bad and Bax. Furthermore, EPO treatment enhanced the expression of p-ERK, p-p53, Bcl-2, and Bcl-xl with no influence on the expression of EPOR, ERK, and p53.
CONCLUSIONS
These findings demonstrated that EPO pretreatment can attenuate renal IR injury by inhibiting apoptosis by promoting activation of the ERK/p53 signaling.
背景
细胞凋亡在肾缺血/再灌注（IR）损伤中起重要作用。有证据表明促红细胞生成素（EPO）具有抗凋亡作用。因此，本研究旨在探讨EPO在肾IR损伤中的作用及潜在机制。
方法
通过夹闭大鼠左肾动脉30分钟，随后再灌注24小时，并进行对侧肾切除术，建立肾IR损伤模型。检测肾功能、肾组织学以及EPOR、p-EPOR、ERK、p-ERK、p-p53、p53、Bcl-2、Bcl-xl、Bad和Bax的表达。
结果
EPO预处理显著降低了肾功能障碍、病理变化以及Bad和Bax的表达。此外，EPO处理增强了p-ERK、p-p53、Bcl-2和Bcl-xl的表达，而对EPOR、ERK和p53的表达无影响。
结论
这些发现表明，EPO预处理可通过促进ERK/p53信号通路的激活来抑制细胞凋亡，从而减轻肾IR损伤。
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