Hydrogen‑rich medium alleviates high glucose‑induced oxidative stress and parthanatos in rat Schwann cells in vitro.

Diabetic peripheral neuropathy (DPN) is considered to be the most common cause of microvascular diabetic complications, for which no effective therapies currently exist. Previous studies have identified that oxidative stress is the common pathway in all possible hypotheses for the induction of DPN, and poly(ADP‑ribose) (PAR) polymerase‑1 (PARP‑1)‑dependent cell death (parthanatos) is key in the pathogenic mechanisms of neurodegenerative disease. The aim of the present study was to investigate the protective effects and corresponding mechanisms of hydrogen‑rich medium (HM) on high glucose (HG)‑induced oxidative stress and parthanatos in primary rat Schwann cells (RSCs) in vitro. The RSCs were divided into groups and treated for 48 h. Cell counting kit‑8 and lactate dehydrogenase assays were used to detect cell viability and cytotoxicity, respectively; intracellular OH‑ levels were measured using a DCFH‑DA assay; concentrations of peroxynitrite (ONOO‑) and 8‑hydroxy deoxyguanosine (8‑OHdG) were evaluated with an enzyme‑linked immunosorbent assay; relative expression levels of parthanatos‑related proteins [PAR, nucleus apoptosis‑inducing factor (AIF) and total AIF] were analyzed using western blot analysis, and immunofluorescence was used to determine the nuclear translocation of AIF. After 48 h, HG was shown to induce severe oxidative stress and promote marked levels of parthanatos in the RSCs. Treatment with HM inhibited HG‑induced oxidative stress by reducing the production of OH‑ and ONOO‑ and suppressed parthanatos by downregulating the levels of 8‑OHdG, the expression of PAR and the nuclear translocation of AIF. HM improved cell viability and inhibited cytotoxicity under the HG condition. These results indicate that HM effectively reduces HG‑induced oxidative stress in RSCs and protects them against parthanatos. Therefore, HM may be a novel treatment for DPN.