Hydrogen-rich water demonstrates significant neuroprotective effects in traumatic brain injury by reducing pro-inflammatory cytokines, decreasing brain edema, and improving blood-brain barrier integrity while enhancing survival rates in rat models. The therapeutic mechanism involves both anti-inflammatory and antioxidant pathways, suggesting hydrogen-rich water as a promising therapeutic intervention for TBI patients. These findings support further clinical investigation of hydrogen therapy as an adjunctive treatment strategy for traumatic brain injury management.
Plain-Language Summary
Researchers gave rats with traumatic brain injuries (TBI) either hydrogen-rich water or regular water to see if it would help reduce brain damage. Rats that received hydrogen-rich water showed better survival rates, less brain swelling, better blood-brain barrier function (a protective layer around the brain), and improved neurological function compared to the control group. The hydrogen-rich water also reduced inflammatory markers (chemical signals that cause inflammation) in the brain tissue.
Abstract
Inflammation and oxidative stress are the two major causes of apoptosis after traumatic brain injury (TBI). Most previous studies of the neuroprotective effects of hydrogen-rich water on TBI primarily focused on antioxidant effects. The present study investigated whether hydrogen-rich water (HRW) could attenuate brain damage and inflammation after traumatic brain injury in rats. A TBI model was induced using a controlled cortical impact injury. HRW or distilled water was injected intraperitoneally daily following surgery. We measured survival rate, brain edema, blood-brain barrier (BBB) breakdown and neurological dysfunction in all animals. Changes in inflammatory cytokines, inflammatory cells and Cho/Cr metabolites in brain tissues were also detected. Our results demonstrated that TBI-challenged rats exhibited significant brain injuries that were characterized by decreased survival rate and increased BBB permeability, brain edema, and neurological dysfunction, while HRW treatment ameliorated the consequences of TBI. HRW treatment also decreased the levels of pro-inflammatory cytokines (TNF-α, IL-1β and HMGB1), inflammatory cell number (Iba1) and inflammatory metabolites (Cho) and increased the levels of an anti-inflammatory cytokine (IL-10) in the brain tissues of TBI-challenged rats. In conclusion, HRW could exert a neuroprotective effect against TBI and attenuate inflammation, which suggests HRW as an effective therapeutic strategy for TBI patients.
