Hydrogen Water Improves Survival in Transplant Complications Study
- Authors
- Li-Ren Qian, Jiaxin Liu, Weina Ma, Yu Liu, Xiaona Wang, Daihong Liu
- Journal
- Oxidative Medicine and Cellular Longevity
- Year
- 2021
- DOI
- 10.1155/2021/1165928
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Chronic Graft-versus-Host Disease
- Body System
- Immune System
TL;DR
Drinking hydrogen-rich water improved survival and reduced symptoms in a mouse model of a serious post-transplant complication.
Key Finding
Mice with chronic graft-versus-host disease that received hydrogen-rich water had a 93.3% survival rate compared to 66.7% in untreated mice, along with significantly improved skin symptoms and reduced markers of cellular damage.
Summary
Researchers tested whether hydrogen-rich water could help mice with chronic graft-versus-host disease (cGVHD), a serious complication that occurs after bone marrow transplants. Mice that drank hydrogen-rich water had better survival rates, improved skin symptoms, and showed signs of reduced cellular damage compared to mice that didn't receive it. The improvement appeared to work by reducing oxidative stress (cellular damage from harmful molecules) and preventing cell death.
Practical Takeaway
This early-stage mouse study suggests hydrogen-rich water may help with graft-versus-host disease complications after bone marrow transplants, but these results cannot yet be applied to humans. Much more research, including clinical trials in transplant patients, would be needed before hydrogen-rich water could be considered a treatment option for this serious condition.
Abstract
Background. Allogeneic hematopoietic stem cell transplantation (allo‐HSCT) is an important treatment option for various hematopoietic diseases and certain hereditary diseases. Chronic graft‐versus‐host disease (cGVHD) has become the main life‐threatening complication and cause of death in later stage postallo‐HSCT. Current treatment options for cGVHD are limited. Hydrogen gas (H2) has been demonstrated that has antioxidative, anti‐inflammatory, and antifibrosis effects. The aim of this study was to confirm whether oral administration hydrogen‐rich water exerted therapeutic effects on a scleroderma cGVHD mouse model and tried to explain the mechanism underly it. Methods. A mouse cGVHD model was established by haploidentical bone marrow transplantation. To evaluate therapeutic effects of H2 on cGVHD, survival rate, changes in clinical scores, and skin pathologic characteristics of cGVHD mice were observed. To evaluate its therapeutic mechanism, we detected the expression levels of antioxidative enzymes heme oxygenase‐1(HO‐1) and NAD (P)H: quinone acceptor oxidoreductase 1(NQO1) in skin homogenates. We also detected the expression level of the apoptotic protein caspase‐3 in skin homogenates. Results. 1‐month survival rate of cGVHD mice in the hydrogen group reached 93.3%, significantly higher than 66.7% in the nonhydrogen group (p < 0.05). Clinical score of cGVHD mice was improved by hydrogen‐rich water at 96 days posttransplantation (2.2 versus 4.5, p < 0.05). The skin pathological condition of cGVHD mice was significantly improved by hydrogen‐rich water. At 96 days posttransplantation, average skin pathological hematoxylin and eosin (HE) staining score in the hydrogen group was 1.05, which was significantly lower than 3.2 in the nonhydrogen group (p < 0.01). Average Masson staining score was 0.6 point in the hydrogen group, lower than 0.9 point in the nonhydrogen group (p < 0.05). Both the relative expression levels of HO‐1 and NQO1 proteins in skin specimens of cGVHD mice in the hydrogen group were lower than that in the nonhydrogen group (2.47 versus 6.21 and 1.83 versus 3.59, p < 0.05). The relative expression level of caspase‐3 protein in skin specimens of cGVHD mice increased to 7.17 on the 96th day after transplantation, significantly higher than 4.36 in the hydrogen group. Conclusion. In this study, we found that oral hydrogen‐rich water improved the survival rate and clinical symptoms of cGVHD mice by antioxidant and antiapoptosis. This study would pave the way for further clinical study, which may provide a new treatment option for cGVHD.