Hydrogen gas ameliorates acute alcoholic liver injury via anti-inflammatory and antioxidant effects and regulation of intestinal microbiota

Alcoholic liver disease (ALD) is a globally prevalent liver-related disorder characterized by severe oxidative stress and inflammatory liver damage, for which no effective treatment is currently available. Hydrogen gas (H2) has been demonstrated to be an efficient antioxidant in various diseases in animals as well as humans. However, the protective effects of H2 on ALD and its underlying mechanisms remain to be elucidated. The present study demonstrated that H2 inhalation ameliorated liver injury, and attenuated liver oxidative stress, inflammation, and steatosis in an ALD mouse model. Moreover, H2 inhalation improved gut microbiota, including increasing the abundance of Lachnospiraceae and Clostridia, and decreasing the abundance of Prevotellaceae and Muribaculaceae, and also improved intestinal barrier integrity. Mechanistically, H2 inhalation blocked activation of the LPS/TLR4/NF-κB pathway in liver. Notably, it was further demonstrated that the reshaped gut microbiota may accelerate alcohol metabolism, regulate lipid homeostasis and maintain immune balance by bacterial functional potential prediction (PICRUSt). Fecal microbiota transplantation from mice that had undergone H2 inhalation significantly alleviated acute alcoholic liver injury. In summary, the present study showed that H2 inhalation alleviated liver injury by reducing oxidative stress and inflammation, while also improving intestinal flora and enhancing the intestinal barrier. H2 inhalation may serve as an effective intervention for preventing and treating ALD in a clinical context.

Retracted: Hydrogen alleviates collagen-induced arthritis (CIA) in mice by inhibiting IL-22 levels

Objective To investigate the therapeutic effect and mechanism of hydrogen (H2) on collagen-induced arthritis (CIA) in mice. Methods DBA/1 mice were randomly divided into normal control group, CIA group and CIA mice treated with H2 group (H2 treated group), with 6 mice in each group. Following the preparation of CIA mouse model, the H2 treated group received H2 inhalation therapy (300 mL/L, 3 hours/d) for 15-60 days. The arthritis score were assessed and HE staining of joint were evaluated by referring to the pathology score; The number of CD4+IL-22+ cells in spleen and joint was observed by flow cytometry and immunohistochemical staining; ELISA was conducted to assess the levels of interleukin 22 (IL-22) in serum and joint; Western blotting was performed to examine the expression of phosphorylated STAT3 (p-STAT3) and phosphorylated NF-κB (p-NF-κB) in joint between the three groups. Results In the CIA group, both the arthritis score and pathology score were higher than control group, while they dropped after H2 treatment. In addition, compared with control group, CIA group showed higher proportion of CD4+IL-22+ cells and higher level of IL-22 which then interestingly decreased after H2 therapy. Besides, the p-STAT3 and p-NF-κB were elevated in CIA mice compared with control group, and H2 treatment significantly inhibited them. Conclusion H2 can reduce the levels of CD4+IL-22+ cells and IL-22, and alleviate arthritis symptoms in CIA mice by inhibiting STAT3/NF-κB pathway.