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

被引:17
作者
Sun, Qian [1 ]
Shen, Zi-Ying [2 ]
Duan, Wei-Na [1 ]
Meng, Qing-Tao [1 ]
Xia, Zhong-Yuan [1 ]
机构
[1] Wuhan Univ, Dept Anesthesiol, Renmin Hosp, 238 Jiefang Rd, Wuhan 430060, Hubei, Peoples R China
[2] Qingdao Univ, Med Coll, Affiliated Hosp, Dept Anesthesiol, Qingdao 266003, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
DJ-1; nuclear factor erythroid 2-related factor-2; acute kidney injury; myocardial ischemia-reperfusion; diabetes; ISCHEMIA-REPERFUSION INJURY; OXIDATIVE STRESS; CARDIAC-SURGERY; RENAL DAMAGE; NITRIC-OXIDE; HYPERGLYCEMIA; NEPHROPATHY; ACTIVATION; RISK; DJ-1;
D O I
10.3892/etm.2017.5095
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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 beta 2-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.
引用
收藏
页码:4201 / 4207
页数:7
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