Mechanism of myocardial ischemia/reperfusion‑induced acute kidney injury through DJ‑1/Nrf2 pathway in diabetic rats

Sun,Qian; Shen,Zi‑Ying; Duan,Wei‑Na; Meng,Qing‑Tao; Xia,Zhong‑Yuan

doi:10.3892/etm.2017.5095

Mechanism of myocardial ischemia/reperfusion‑induced acute kidney injury through DJ‑1/Nrf2 pathway in diabetic rats

Authors:
- Qian Sun
- Zi‑Ying Shen
- Wei‑Na Duan
- Qing‑Tao Meng
- Zhong‑Yuan Xia
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Affiliations: Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China, Department of Anesthesiology, The Affiliated Hospital of The Medical College of Qingdao University, Qingdao, Shandong 266003, P.R. China
Published online on: September 1, 2017 https://doi.org/10.3892/etm.2017.5095
Pages: 4201-4207
Copyright: © Sun et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The objective of the present study was to investigate acute kidney injury (AKI) induced by myocardial ischemia/reperfusion (MIR) in diabetic rats and elucidate its underlying mechanism. A rat model of MIR was established by left anterior descending coronary artery occlusion for 30 min, followed by reperfusion for 2 h. Rats were randomly divided into four groups: i) Sham group, ii) sham + MIR group, iii) diabetic group and iv) diabetes + MIR group. Myocardial injury was detected by plasma creatine kinase isoenzyme MB and lactate dehydrogenase assays. AKI induced by MIR in diabetic rats was characterized by increases in cystatin C and β2‑microglobulin levels. Oxidative stress injury was accompanied by an increase of malondialdehyde levels and a decrease of total antioxidative capacity in the renal tissues. Immunohistochemistry and western blot analysis demonstrated that the expression of DJ‑1 and nuclear factor erythroid 2‑related factor 2 (Nrf2) were significantly increased in the diabetes + MIR group compared with that in the sham + MIR and diabetic groups. Taken together, these results suggested that AKI induced by MIR in diabetic rats may be associated with activation of the DJ‑1/Nrf2 pathway.

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