Hydrogen Gas Prevents Bone Loss in Postmenopausal Osteoporosis Study

Authors
Journal
Menopause
Year
DOI
10.1097/GME.0000000000001310
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Osteoporosis
Body System
Skeletal

TL;DR

Hydrogen gas (H2) treatment significantly reduced bone loss and inflammation in mice with osteoporosis-like conditions.

Key Finding

Mice that inhaled hydrogen gas had more than 40% higher bone mineral density and trabecular bone volume compared to untreated mice with ovariectomy-induced bone loss, along with 50% lower levels of inflammatory molecules associated with bone breakdown.

Summary

Researchers tested whether hydrogen gas could help prevent bone loss in mice that had their ovaries removed (a model of postmenopausal osteoporosis). They found that mice breathing 60% hydrogen gas had significantly stronger bones and higher bone density than mice breathing regular air, and their levels of inflammatory molecules linked to bone loss were much lower. The hydrogen appeared to work by blocking a cellular pathway (NF-κB) that normally triggers bone-dissolving cells to become active.

Practical Takeaway

This mouse study suggests hydrogen gas may help prevent bone loss related to menopause, but it is early-stage research in animals only. Human studies would be needed to determine whether these results apply to people and whether inhaling hydrogen gas is a practical or safe treatment option for osteoporosis.

Abstract

AbstractObjectives:Osteoporosis is a prevalent condition among postmenopausal women, and lacks satisfactory therapeutic options. Hydrogen (H2) has been shown to be effective in alleviating many diseases. This study aimed to investigate the effects of H2on inhibiting osteoclastogenesis and bone loss in ovariectomized mice.Methods:Osteoclast differentiation from Raw264.7 cells was induced with receptor activator NF-κB ligand (RANKL) with or without 60% H2. The number and resorption activity of osteocalsts were assessed by tartrate-resistant acid phosphatase staining and pit formation assay, respectively. The expression of osteoclast markers and NF-κB phosphorylation were detected by western blot. NF-κB nuclear translocation was assessed by immunofluorescence. NF-κB transcriptional activity was analyzed by luciferase assay. Bone loss in mice was induced by ovariectomy (OVX). OVX mice were given either regular air or 60% H2. Bone structure was analyzed by micro-computed tomography and hematoxylin and eosin staining. Cytokine levels were measured by enzyme-linked immunosorbent assay. The data were analyzed with one-way or two-way ANOVA followed by Bonferroni post hoc tests.Results:H2did not have any measurable effect on the proliferation of Raw264.7 cells. The number of osteoclasts and size of resorption pits of RANKL+H2-treated cells were 3 to 4 times less than RANKL treated cells. The expression of osteoclast marker genes of RANKL+H2-treated cells was 30% to 60% lower than RANKL-treated cells (P< 0.05). H2markedly inhibited RANKL-induced activation, nuclear translocation, and transcriptional activity of NF-κB (P < 0.05, RANKL+H2vs RANKL). The amount and density of trabecular bone and bone mineral density of ovariectomized mice were significantly less than sham-operated mice (P < 0.05 OVX vs sham). The amount of trabecular bone and bone mineral density of OVX mice that inhaled H2were more than 40% higher, whereas the levels of serum proinflammatory cytokine interleukin 1β, IL-6, and tumor necrosis factor-α were more than 50% lower than those of OVX mice (P < 0.05).Conclusions:These results demonstrated that H2could be an effective therapeutic agent of postmenopausal osteoporosis.