期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 50, 期 10, 页码 1314-1323出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2011.02.016
关键词
Oxidative stress; Osteoporosis; Bone formation; MAPK; Reactive oxygen species; Free radicals
资金
- Singapore National Medical Research Council [1183/2008]
Osteoporosis is a bone disease that leads to an increased risk of fracture. Oxidative damage is an important contributor to the morphological and functional changes in the development of osteoporosis. We found in this study that hydrogen sulfide (H2S), a novel endogenous gaseous mediator, protected MC3T3-E1 osteoblastic cells against hydrogen peroxide (H2O2)-induced oxidative injury. NaHS, an H2S donor, increased cell viability and reduced cell apoptosis caused by H2O2. NaHS also stimulated osteoblast proliferation by enhancing both transcription and activity of alkaline phosphatase in MC3T3-E1 osteoblastic cells. Moreover, treatment with NaHS stimulated the transcriptional level of osteocalcin, the main bone matrix protein, and the protein expression of collagen, a major constituent of bone tissue. The above effects were mediated by the antioxidant effect of H2S. NaHS reversed the reduced superoxide dismutase activity, decreased reactive oxygen species production, and suppressed NADPH oxidase activity in H2O2-treated osteoblasts. In addition, NaHS treatment also produced anti-inflammatory effects via inhibition of the production of nitric oxide and TNF-alpha, suggesting an anti-inflammatory effect of H2S. Cell viability and Western blotting analysis demonstrated that the protective effects of H2S were mediated by p38 and ERK1/2 MAPKs. In conclusion, H2S protects osteoblastic cells against oxidative stress-induced cell injury and suppression of proliferation and differentiation via a MAPK (p38 and ERK1/2)-dependent mechanism. Our findings suggest that H2S may have a potentially therapeutic value for osteoporosis. (C) 2011 Elsevier Inc. All rights reserved.
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