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CJAP ›› 2019, Vol. 35 ›› Issue (2): 130-134.doi: 10.12047/j.cjap.5719.2019.029

• ORIGINAL ARTICLES • Previous Articles     Next Articles

Research on the mechanism of high glucose affecting the apoptosis of schwann cells by Nox4 NADPH oxidase

YU Ting1 , XIN Qing1 , XU Fei2, LI Lei3△   

  1. 1. Department of Physiology, Jining Medical University, Jining 272067;
    2. Department of Vascular Surgery, Jining First People's Hospital, Jining 272011;
    3. Department of Neurology, Affiliated Hospital of Jining Medical University, Jining 272029, China
  • Online:2019-03-28 Published:2019-06-27

Abstract: Objective: To investigate the mechanism of high glucose affecting the apoptosis of schwann cells through Nox4 NADPH oxidase. Methods: The schwann cells of newborn Wistar rats were cultured in vitro. The cultured cells were divided into four groups: control group, high-glucose group, NOX4 siRNA group and control siRNA group (n=10). The WST-1 method was used to detect the cell vitality, and the DCFH-DA method was used to detect the contents of intracellular reactive oxygen free radicals (ROS). Nox4 and Caspase3 mRNA expressions were detected by real-time fluorescence quantitative RT-PCR. Nox4 and Caspase3 protein expressions were determined by Western blot. Results: High glucose culture up-regulated Nox4 mRNA and protein expressions of schwann cells, decreased activity of schwann cells, increased intracellular ROS content, and promoted apoptosis by increasing Caspase3 mRNA and protein expressions. NOX4 siRNA blocked the accumulation of ROS in the high glucose cultured schwann cells, and reduced the damage of glucose on cell viability, by inhibiting NOX4 gene expression. NOX4 siRNA also reduced cell apoptosis by down-regulating Caspase3 mRNA and protein expressions. Conclusion: Nox4 was involved in the hyperglycemic-induced apoptosis of schwann cells through ROS. The regulation of Nox4 expression or function might be a new way to treat diabetic peripheral neuropathy.

Key words: diabetes, schwann cells, NADPH oxidase, reactive oxygen free radicals, apoptosis

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