Hydrogen Therapy Protects Nerves in Diabetic Rats with Nerve Damage

Authors
Journal
Medical Gas Research
Year
DOI
10.4103/2045-9912.345171
Study Type
Rat
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Diabetic Peripheral Neuropathy
Body System
Nervous System

TL;DR

Breathing in hydrogen gas can significantly reduce blood sugar and nerve damage in rats with diabetes-induced nerve pain.

Key Finding

Hydrogen inhalation significantly improved nerve function in diabetic rats and reduced oxidative stress markers by activating a protective cellular pathway called Nrf2.

Summary

This study tested whether hydrogen could help protect nerves damaged by diabetes in rats. Researchers gave diabetic rats either hydrogen gas to breathe or hydrogen-rich saline, then measured nerve function and markers of cellular damage (oxidative stress). Hydrogen inhalation reduced blood sugar levels, improved nerve signal speed, and decreased harmful molecules in nerve tissue while boosting the body's natural antioxidant defenses.

Practical Takeaway

This early-stage animal study suggests hydrogen may help protect nerves from diabetes-related damage, but human studies are needed before any conclusions can be drawn about its use in people. The findings are limited to rats and do not yet demonstrate that hydrogen would have the same effects in humans with diabetic neuropathy.

Abstract

Diabetic peripheral neuropathy (DPN) is a complex disorder caused by long-standing diabetes. Oxidative stress was considered the critical creed in this DPN pathophysiology. Hydrogen has antioxidative effects on diabetes mellitus and related complications. However, there is still no concern on the beneficial effects of hydrogen in DPN. This paper aimed to evaluate the effects of exogenous hydrogen to reduce the severity of DPN in streptozotocin-induced diabetic rats. Compared with hydrogen-rich saline treatment, hydrogen inhalation significantly reduced blood glucose levels in diabetic rats in the 4th and 8th weeks. With regard to nerve function, hydrogen administration significantly attenuated the decrease in the velocity of motor nerve conduction in diabetic animals. In addition, hydrogen significantly attenuated oxidative stress by reducing the level of malondialdehyde, reactive oxygen species, and 8-hydroxy-2-deoxyguanosine and meaningfully enhanced the antioxidant capability by partially restoring the activities of superoxide dismutase. Further studies showed that hydrogen significantly upregulated the expression of nuclear factor erythroid-2-related factor 2 and downstream proteins such as catalase and hemeoxygenase-1 in the nerves of diabetic animals. Our paper showed that hydrogen exerts significant protective effects in DPN by downregulating oxidative stress via the pathway of nuclear factor erythroid-2-related factor 2, which suggests its potential value in clinical applications.