Can hydrogen water help with traumatic brain injury?

This rat study suggests hydrogen water may help protect the brain after traumatic injury by reducing inflammation and cell damage. The hydrogen-treated rats showed better neurological recovery and less brain tissue damage compared to untreated rats.

How does hydrogen water protect the brain after injury?

Hydrogen water appears to work by reducing harmful molecules called reactive oxygen species and protecting mitochondria (cell energy factories). It also decreases inflammatory proteins like TNF-α and IL-1β that contribute to brain damage after trauma.

What did this brain injury study find about hydrogen therapy?

The study found that rats treated with hydrogen water had significantly better neurological recovery scores and less brain damage. Laboratory tests showed reduced inflammation, less cell death, and better preservation of brain cell function.

How was hydrogen water given to the rats in this study?

The researchers gave rats daily injections of hydrogen-rich water (5 mL/kg body weight) starting immediately after the brain injury. Treatment continued until the rats were studied at 1, 3, or 7 days after injury.

Is hydrogen water safe for brain injury patients?

While this rat study showed no apparent side effects, human safety and effectiveness have not been established for brain injury treatment. More research is needed before hydrogen water can be recommended for traumatic brain injury patients.

Hydrogen Water Protects Brain After Traumatic Injury in Rats

Authors: Jiangquan Fu, Qing Lan, Difen Wang, Ying Wang, Ying Liu
Journal: Chinese Critical Care Medicine
Year: 2018
DOI: 10.3760/cma.j.issn.2095-4352.2018.04.006
Study Type: Rat
Outcome: Positive
Peer Reviewed: Yes
Country: China
Health Condition: Traumatic Brain Injury
Body System: Nervous System

TL;DR

Injecting hydrogen-rich water into rats after a traumatic brain injury reduces brain cell damage and inflammation, improving brain function.

Key Finding

In rats with traumatic brain injury, hydrogen-rich water treatment reduced neurological damage scores and decreased inflammatory markers and mitochondrial damage compared to untreated injured rats.

Summary

Researchers gave rats with traumatic brain injuries (TBI) hydrogen-rich water through injection and compared them to rats with TBI who received regular saline. Hydrogen-rich water treatment reduced neurological damage scores, lowered inflammatory markers (TNF-α and IL-1β) in brain tissue, decreased harmful reactive oxygen species (unstable molecules that damage cells), and preserved mitochondrial function (the energy-producing structures in cells). These improvements suggest hydrogen-rich water may protect brain cells from further damage after injury.

Practical Takeaway

This rat study suggests hydrogen-rich water may have neuroprotective effects after traumatic brain injury by reducing inflammation and cellular damage. However, these findings are from animal studies only and cannot be directly applied to humans; clinical trials in people would be needed to determine if similar benefits occur. The practical relevance for consumers remains unclear until human research is conducted.

Abstract

Objective: To observe the effect of hydrogen-rich water on the chondriosome damage and cytokines change in brain tissue of rats with traumatic brain injury (TBI). Methods: Fifty-four health male Sprague-Dawley (SD) rats were divided into three groups by random number table: sham group, trauma group (TBI group), and trauma+hydrogen-rich water group (TBI+HW group), the rats in each group were subdivided into 1, 3 and 7 days subgroups according to the time points after trauma, with 6 rats in each subgroup. The TBI model was reproduced by using a modified Feency method for free fall impact, and the rats in sham group were not given brain impact after craniotomy. The rats in TBI+HW group were given intraperitoneal injection of hydrogen-rich water (5 mL/kg) after TBI model reproduction, and then once a day until being sacrificed; and the rats in sham group and TBI group were given the same amount of normal saline. The neurological severity scores (NSS) for neurologic deficits were calculated at corresponding time points, and then the rats were sacrificed to harvest brain tissue at 3 mm around lesion boundary. The cytokines including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were determined by enzyme linked immunosorbent assay (ELISA); the protein expressions of Bax, Bcl-2 were determined by Western Blot; the RFU of reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and mitochondrial membrane permeability (MPTP) were determined by fluorescence and enzyme sign method. Results: TBI and TBI+HW groups appeared obvious neurologic damage after injury in rats. NSS scores in TBI and TBI+HW groups showed a decreased tendency with time prolongation after TBI. NSS scores in TBI+HW group at 3 days and 7 days were significantly lower than those of TBI group (NSS score: 9.67±0.82 vs. 11.17±1.17, 6.83±0.75 vs. 8.50±1.04, both P < 0.05). Compared with sham group, the expressions of TNF-α, IL-1β, RFU of ROS in chondriosome, protein expression of Bax in brain tissue in TBI group and TBI+HW group were significantly increased, peaked at 1 day, then they gradually declined. Each time point of RFU of MMP, MPTP in chondriosome and protein expression of Bcl-2 were significantly decreased, and gradually increased after one-day valley value. Compared with TBI group, the expressions of TNF-α, IL-1β, RFU of ROS in chondriosome and protein expression of Bax in brain tissue were all declined at corresponding time points [TNF-α (ng/L): 54.14±1.11 vs. 81.49±2.76, IL-1β (ng/L): 74.53±1.75 vs. 119.44±3.56, ROS (RFU): 92.30±2.46 vs. 121.33±6.57, Bax: 0.89±0.01 vs. 1.10±0.01, all P < 0.01]; RFU of MMP, MPTP in chondriosome and the protein expression of Bcl-2 were all increased at corresponding time points [MMP (RFU): 99.28±3.97 vs. 74.72±3.00, MPTP (RFU): 188.82±4.44 vs. 160.01±2.04, Bcl-2: 0.52±0.02 vs. 0.30±0.02, all P < 0.01]. Conclusions: The high expressions of cytokines and chondriosome damage were involved in the early TBI. Early treatment with an intraperitoneally injection of hydrogen-rich water can reduce chondriosome damage and inflammation factor release, reduce the nerve cell apoptosis after TBI, and protect brain function.