Is myeloperoxidase a key component in the ROS-induced vascular damage related to nephropathy in type 2 diabetes?

髓过氧化物酶是否是 ROS 诱发的 2 型糖尿病肾病相关血管损伤的关键成分?

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作者:Susana Rovira-Llopis, Milagros Rocha, Rosa Falcon, Carmen de Pablo, Angeles Alvarez, Ana Jover, Antonio Hernandez-Mijares, Victor M Victor

Abstract

It is still unclear whether microvascular complications of type 2 diabetes correlate with leukocyte-endothelium interactions and/or myeloperoxidase (MPO) levels. In the present study, we found that serum levels of glucose, the rate of ROS and MPO concentration were higher in type 2 diabetic patients. Patients with nephropathy (39.6%) presented higher MPO levels that correlate positively with the albumin/creatinine ratio (r = 0.59, p<0.05). In addition, nephropatic patients showed increased leukocyte-endothelium interactions due to an undermining of polymorphonuclear leukocytes (PMN) rolling velocity and increased rolling flux and adhesion, which was accompanied by a rise in levels of the proinflammatory cytokine tumour necrosis factor alpha (TNFα) and the adhesion molecule E-selectin. Furthermore, MPO levels were positively correlated with PMN rolling flux (r = 0.855, p < 0.01) and adhesion (r = 0.682, p<0.05). Our results lead to the hypothesis that type 2 diabetes induces oxidative stress and an increase in MPO levels and leukocyte-endothelium interactions, and that these effects correlate with the development of nephropathy.

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