Positive Effects of Hydrogen Water on 2,4-Dinitrochlorobenzene-Induced Atopic Dermatitis in NC/Nga Mice

Abstract

Atopic dermatitis (AD) is a chronically relapsing, pruritic, eczematous skin disorder accompanying al- lergic inflammation. AD is triggered by oxidative stress and immune imbalance. In the present study, we in- vestigated the effect of drinking hydrogen water (HW) on 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis in NC/Nga mice and found that HW ameliorated DNCB-induced AD-like clinical symptoms. In line with this, the level of reactive oxygen species in the HW group was significantly inhibited compared with that in the purified water (PW) group. In parallel, HW enhanced glutathione peroxidase activity in DNCB- induced AD as compared with the PW group. Accordingly, the levels of thymus and activation-regulated chemokine and cytokines were significantly decreased in the HW group compared with the PW group. Nota- bly, the levels of Th2 cytokine, interleukin-5 (IL-5), and proinflammatory cytokines such as tumor necrosis factor-α and IL-6 in HW-fed mice were significantly lower than in control and PW-fed mice. The total serum immunoglobulin E level was also markedly reduced in the HW group. The collective results indicate that HW suppresses DNCB-induced AD in NC/Nga mice via redox balance and immune modulation and could be a safe clinical fluid treatment for AD.

Study details

Article type

Original Research

Disease / injury model

2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis in NC/Nga mice

Duration

12 weeks

Dose comparison

Only one concentration of hydrogen water (1.5 ppm) was used; no dose comparison was performed.

Dose-dependent effect

No

Outcome

Positive

Findings

Hydrogen water (HW) ameliorated DNCB-induced atopic dermatitis-like symptoms in NC/Nga mice, significantly reduced scratching behavior, decreased serum reactive oxygen species (ROS), increased glutathione peroxidase (GPx) activity, lowered levels of Th2 cytokine (IL-5), pro-inflammatory cytokines (TNF-α, IL-6), chemokine (TARC), and total serum IgE, indicating suppression of AD via redox balance and immune modulation.