Hydrogen-rich water attenuates brain damage and inflammation after traumatic brain injury in rats.

Abstract

Traumatic brain injury (TBI) triggers both oxidative stress and neuroinflammation, which together drive post-injury apoptosis. This rat study examined the effects of intraperitoneally administered hydrogen-rich water (HRW) following controlled cortical impact-induced TBI. Outcome measures included survival rate, brain edema, blood-brain barrier (BBB) permeability, and neurological function. TBI-challenged animals showed markedly reduced survival, elevated BBB permeability, pronounced edema, and impaired neurological performance. HRW administration significantly reversed these outcomes. At the molecular level, pro-inflammatory cytokines TNF-α, IL-1β, and HMGB1 were reduced, microglial activation marker Iba1 and the inflammatory metabolite choline (Cho) were decreased, and the anti-inflammatory cytokine IL-10 was elevated in brain tissue. These findings indicate that HRW exerts neuroprotective effects in TBI partly through suppression of neuroinflammatory cascades, extending beyond previously documented antioxidant mechanisms.

Mechanism

HRW reduces pro-inflammatory cytokines (TNF-α, IL-1β, HMGB1) and microglial activation (Iba1) while elevating anti-inflammatory IL-10 in injured brain tissue, thereby suppressing neuroinflammation and attenuating blood-brain barrier disruption and edema following TBI.