Hydrogen Treatment Protects Nerve Cells from Diabetes Damage
- Authors
- Qing Li, Yang Jiao, Yang Yu, Guolin Wang, Yong-Hao Yu
- Journal
- Molecular Medicine Reports
- Year
- 2018
- DOI
- 10.3892/mmr.2018.9631
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Diabetic Peripheral Neuropathy
- Body System
- Nervous System
TL;DR
A hydrogen-rich solution can protect nerve cells from damage caused by high blood sugar in diabetes.
Key Finding
Hydrogen-rich medium reduced oxidative stress and prevented PARP-1-dependent cell death in rat Schwann cells exposed to high glucose levels in laboratory conditions.
Summary
Researchers tested whether hydrogen-rich water could protect nerve support cells (called Schwann cells) from damage caused by high glucose levels in a laboratory dish. They found that hydrogen-rich medium reduced harmful molecules called free radicals and prevented a type of cell death triggered by a protein called PARP-1, while also improving cell survival under high-glucose conditions.
Practical Takeaway
This is an early laboratory study in rat cells only, not humans. While the results suggest hydrogen-rich water may help protect nerve cells from high-glucose damage, much more research—including animal studies and human trials—would be needed before any conclusions about its usefulness for diabetic nerve damage could be drawn.
Abstract
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.