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Erythropoietin pretreatment ameliorates renal ischaemia-reperfusion injury by activating PI3K/Akt signalling.
Nephrology (Carlton). 2015 Apr; 20(4):266-72.N

Abstract

AIM

Renal ischaemia-reperfusion (I/R) injury, a primary cause of acute renal failure, can induce high morbidity and mortality. This study aimed to explore the effect of erythropoietin on renal I/R injury and its underlying mechanism.

METHODS

Fifty male Sprague-Dawley rats were randomly allocated to three groups (n = 10): the sham group, the renal ischaemia-reperfusion-saline (IRI) group, and the IRI+-Erythropoietin (EPO) group. Erythropoietin (250, 500, 1000 U/kg) was intraperitoneally injected 30 min before inducing I/R. Renal I/R injury were induced by clamping the left renal artery for 30 min followed by reperfusion, along with a contralateral nephrectomy. Renal function and histological damage were determined after 24 h reperfusion. The expression of pro-inflammatory cytokines interleukin-6 (IL-6), interleukin-1 β (IL-1β), and tumour necrosis factor-α (TNF-α) in the serum and renal tissue were evaluated by enzyme linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR), respectively. Further, the effects of erythropoietin on PI3K/Akt signalling, erythropoietin receptor (EPOR) and nuclear factor (NF)-κB activation were measured by Western blotting.

RESULTS

Erythropoietin pretreatment can significantly decrease the level of renal dysfunction in a dose-dependent manner, attenuated the renal histological changes, the expression of TNF-α, IL-1β, and IL-6, the levels of reactive oxygen species (ROS) production and NF-κB p65 phosphorylation in renal tissue upon IRI. Moreover, erythropoietin pretreatment could further activate the PI3K/Akt signalling and induced EPOR activity.

CONCLUSIONS

Erythropoietin pretreatment could attenuate renal I/R injury by suppressing inflammation, which was associated with activating PI3K/Akt signalling though EPOR activation. Our findings suggest that erythropoietin may be a novel practical strategy to prevent renal I/R injury.

Authors+Show Affiliations

Department of Nephrology, University of Electronic Science and Technology, Sichuan Academy of Sciences & Sichuan Provincial People's Hospital, Chengdu, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25581532

Citation

Zhang, Jiong, et al. "Erythropoietin Pretreatment Ameliorates Renal Ischaemia-reperfusion Injury By Activating PI3K/Akt Signalling." Nephrology (Carlton, Vic.), vol. 20, no. 4, 2015, pp. 266-72.
Zhang J, Zou YR, Zhong X, et al. Erythropoietin pretreatment ameliorates renal ischaemia-reperfusion injury by activating PI3K/Akt signalling. Nephrology (Carlton). 2015;20(4):266-72.
Zhang, J., Zou, Y. R., Zhong, X., Deng, H. D., Pu, L., Peng, K., & Wang, L. (2015). Erythropoietin pretreatment ameliorates renal ischaemia-reperfusion injury by activating PI3K/Akt signalling. Nephrology (Carlton, Vic.), 20(4), 266-72. https://doi.org/10.1111/nep.12384
Zhang J, et al. Erythropoietin Pretreatment Ameliorates Renal Ischaemia-reperfusion Injury By Activating PI3K/Akt Signalling. Nephrology (Carlton). 2015;20(4):266-72. PubMed PMID: 25581532.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Erythropoietin pretreatment ameliorates renal ischaemia-reperfusion injury by activating PI3K/Akt signalling. AU - Zhang,Jiong, AU - Zou,Yu-Rong, AU - Zhong,Xiang, AU - Deng,Hanlu Ding Fei, AU - Pu,Lei, AU - Peng,Kun, AU - Wang,Li, PY - 2014/12/16/accepted PY - 2015/1/13/entrez PY - 2015/1/13/pubmed PY - 2015/12/22/medline KW - PI3K/Akt KW - erythropoietin KW - renal ischaemia reperfusion injury SP - 266 EP - 72 JF - Nephrology (Carlton, Vic.) JO - Nephrology (Carlton) VL - 20 IS - 4 N2 - AIM: Renal ischaemia-reperfusion (I/R) injury, a primary cause of acute renal failure, can induce high morbidity and mortality. This study aimed to explore the effect of erythropoietin on renal I/R injury and its underlying mechanism. METHODS: Fifty male Sprague-Dawley rats were randomly allocated to three groups (n = 10): the sham group, the renal ischaemia-reperfusion-saline (IRI) group, and the IRI+-Erythropoietin (EPO) group. Erythropoietin (250, 500, 1000 U/kg) was intraperitoneally injected 30 min before inducing I/R. Renal I/R injury were induced by clamping the left renal artery for 30 min followed by reperfusion, along with a contralateral nephrectomy. Renal function and histological damage were determined after 24 h reperfusion. The expression of pro-inflammatory cytokines interleukin-6 (IL-6), interleukin-1 β (IL-1β), and tumour necrosis factor-α (TNF-α) in the serum and renal tissue were evaluated by enzyme linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR), respectively. Further, the effects of erythropoietin on PI3K/Akt signalling, erythropoietin receptor (EPOR) and nuclear factor (NF)-κB activation were measured by Western blotting. RESULTS: Erythropoietin pretreatment can significantly decrease the level of renal dysfunction in a dose-dependent manner, attenuated the renal histological changes, the expression of TNF-α, IL-1β, and IL-6, the levels of reactive oxygen species (ROS) production and NF-κB p65 phosphorylation in renal tissue upon IRI. Moreover, erythropoietin pretreatment could further activate the PI3K/Akt signalling and induced EPOR activity. CONCLUSIONS: Erythropoietin pretreatment could attenuate renal I/R injury by suppressing inflammation, which was associated with activating PI3K/Akt signalling though EPOR activation. Our findings suggest that erythropoietin may be a novel practical strategy to prevent renal I/R injury. SN - 1440-1797 UR - https://www.unboundmedicine.com/medline/citation/25581532/Erythropoietin_pretreatment_ameliorates_renal_ischaemia_reperfusion_injury_by_activating_PI3K/Akt_signalling_ L2 - https://doi.org/10.1111/nep.12384 DB - PRIME DP - Unbound Medicine ER -