Protective effect of hydrogenrich medium against high glucoseinduced apoptosis of Schwann cells in vitro

Author:                

Publisher: Spandidos Publications

E-ISSN: 1791-3004|12|3|3986-3992

ISSN: 1791-2997

Source: Molecular Medicine Reports, Vol.12, Iss.3, 2015-01, pp. : 3986-3992

Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.

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Abstract

Diabetic peripheral neuropathy (DPN) is considered to be one of the most prevalent and life threatening microvascular diabetic complications. DPN affects up to 50% of patients with diabetes mellitus and there are currently no efficacious therapeutic strategies available for its treatment. Previous studies have reported that oxidative stress and poly(ADPribose) polymerase1 (PARP1) may be unifying factors for hyperglycemic injury. The aim of the present study was to investigate the protective effects of hydrogenrich medium (HM) on high glucose (HG)mediated oxidative stress, PARP1 activation and the apoptosis of Schwann cells (SCs) in vitro. The cells were divided into different groups, and were treated for 48 h. Cell viability and apoptosis were evaluated using Cell Counting kit8 and annexin V/propidium iodide assays, respectively. The concentrations of 8hydroxy2deoxyguanosine (8OHdG) and peroxynitrite (ONOO) were detected using an enzymelinked immunosorbent assay. The presence of intracellular oxygen free radicals was confirmed using flow cytometric analysis. Colorimetric assays were performed to determine the activity of caspase3, and western blotting was performed to detect the protein expression levels of PARP1, cleaved PARP1, PAR, apoptosisinducing factor (AIF), Bcell lymphoma 2 (Bcl2) and Bcl2associated X protein. HG was found to induce severe oxidative stress and promote the caspasedependent and caspaseindependent apoptosis of SCs. Treatment with HM inhibited HGinduced oxidative stress by suppressing hydroxyl and ONOO production, levels of 8OHdG, caspase3 activity and apoptosis in the SCs. Furthermore, treatment with HM downregulated the HGinduced release of PAR, the activation of PARP1 and nuclear translocation of AIF, and upregulated the expression of Bcl2 in the SCs. These results indicated that HM inhibited the HGinducedoxidative stressassociated caspasedependent and caspaseindependent apoptotic pathways in SCs. Therefore, HM may have potential as a treatment for DPN.