Overexpression of DJ-1 reduces oxidative stress and attenuates hypoxia/reoxygenation injury in NRK-52E cells exposed to high glucose.
Overexpression of DJ-1 reduces oxidative stress and attenuates hypoxia/reoxygenation injury in NRK-52E cells exposed to high glucose.
复制标题
DJ-1 的过度表达可减少暴露于高葡萄糖的 NRK-52E 细胞的氧化应激并减轻缺氧/复氧损伤
DOI：
10.3892/ijmm.2016.2680
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发表时间：
2016-09
影响因子：
5.4
通讯作者：
Chen R
中科院分区：
文献类型：
--
作者：
Shen ZY;Sun Q;Xia ZY;Meng QT;Lei SQ;Zhao B;Tang LH;Xue R;Chen R
糖尿病患者更容易发生肾缺血/再灌注（I/R）损伤，这与高血糖诱导的氧化应激有关。我们以前报道过，高血糖诱导的DJ-1抑制，一种新的癌基因，表现出强大的抗氧化活性，是牵连在心肌I/R损伤的严重程度。本研究旨在探讨DJ-1在高糖诱导的肾细胞缺氧/复氧（H/R）损伤中的作用。为此，NRK-52 E细胞暴露于HG（30 mM）48 h，然后暴露于缺氧4 h和复氧2 h，这显着降低细胞活力和超氧化物歧化酶（SOD）活性，并增加丙二醛（MDA）含量，伴随着DJ-1蛋白表达的减少。DJ-1过表达质粒转染DJ-1过表达对HG诱导的H/R损伤具有保护作用，表现为CCK-8水平和SOD活性增加，乳酸脱氢酶（LDH）释放减少和MDA含量降低，以及核因子（红细胞衍生2）样2（Nrf 2）和血红素加氧酶-1（HO-1）表达增加。用抗氧化剂N-乙酰半胱氨酸处理后观察到类似的效果。这些结果表明DJ-1的过表达降低了暴露于HG的NRK-52 E细胞中的氧化应激并减轻了H/R损伤。
Patients with diabetes are more vulnerable to renal ischemia/reperfusion (I/R) injury, which is implicated in hyperglycemia-induced oxidative stress. We previously reported that the hyperglycemia-induced inhibition of DJ-1, a novel oncogene that exhibits potent antioxidant activity, is implicated in the severity of myocardial I/R injury. In the present study, we aimed to explore the role of DJ-1 in hypoxia/reoxygenation (H/R) injury in renal cells exposed to high glucose (HG). For this purpose, NRK-52E cells were exposed to HG (30 mM) for 48 h and then exposed to hypoxia for 4 h and reoxygenation for 2 h, which significantly decreased cell viability and superoxide dismutase (SOD) activity, and increased the malondialdehyde (MDA) content, accompanied by a decrease in DJ-1 protein expression. The overexpression of DJ-1 by transfection with a DJ-1 overexpression plasmid exerted protective effects against HG-induced H/R injury, as evidenced by increased CCK-8 levels and SOD activity, the decreased release of lactate dehydrogenase (LDH) and the decreased MDA content, and increased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and heme oxygenase-1 (HO-1) expression. Similar effects were observed following treatment with the antioxidant, N-acetylcysteine. These results suggest that the overexpression of DJ-1 reduces oxidative stress and attenuates H/R injury in NRK-52E cells exposed to HG.