Glucocorticoids contribute to the increased incidence of secondary osteoporosis. Hydrogen sulfide (HS) is a gasotransmitter and plays an essential role in bone metabolism. In this study, we investigated the therapeutic effects of HS on glucocorticoid-induced osteoporosis (GIO). We found that dexamethasone (Dex) decreased serum HS and two key HS-generating enzymes in the bone marrow , cystathione b-synthase and cystathione g-lyase. Treatment of HS-donor GYY4137 in rat significantly relieved the inhibitory effect of Dex on bone formation. Dex inhibited osteoblasts proliferation and osteogenic differentiation and decreased the expressions of the two HS-generating enzymes. Further investigation showed that HS was involved in Dex-mediated osteoblasts proliferation, differentiation, and apoptosis. Mechanistically, GYY4137 promoted osteoblastogenesis by activating Wnt signaling through increased production of the Wnt ligands. In comparison, the blockage of Wnt/β-catenin signaling pathway significantly alleviated the effect of HS on osteoblasts. In conclusion, the restoration of HS levels is a potential novel therapeutic approach for GIO.
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| http://dx.doi.org/10.18632/aging.102269 | DOI Listing |
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