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- W3212719347 abstract "Abstract Oxidative stress is an important contributor to the development of osteoporosis. Melatonin, an indoleamine secreted by the pineal gland, has antioxidant properties. This study aims to explore whether melatonin can promote bone formation and elucidate the mechanisms underlying this process. In this study, we used an in vitro hydrogen peroxide (H 2 O 2 )-induced oxidative stress model in MC3T3-E1 cells and an in vivo ovariectomized osteoporotic bone defect model in rats to explore the protective effects of melatonin against osteoporotic bone defects along with the mechanism underlying these effects. We found that melatonin significantly increased alkaline phosphatase activity, mineralization capacity, and the expression of BMP2, RUNX2, and OPN in MC3T3-E1 cells. Furthermore, melatonin was found to activate SIRT1 and inhibit p66SHC, reduce the intracellular reactive oxygen species levels, stabilize mitochondria, reduce malondialdehyde levels, increase superoxide dismutase activity, and reduce apoptosis in MC3T3-E1 cells treated with H 2 O 2 . Intriguingly, these effects could be reversed by the SIRT1 inhibitor EX527. In vivo experiments confirmed that melatonin improves the microstructure and bone mineral density of the distal femoral bone trabecula and promotes bone formation. Taken together, our findings showed that melatonin can restrain oxidative damage in MC3T3-E1 cells via SIRT1/p66SHC pathway and promote osteogenesis, suggesting that melatonin could be a potential therapeutic agent for osteoporosis-related bone metabolic diseases." @default.
- W3212719347 created "2021-11-22" @default.
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- W3212719347 date "2021-10-15" @default.
- W3212719347 modified "2023-09-27" @default.
- W3212719347 title "Melatonin alleviates hydrogen peroxide induced oxidative damage in MC3T3-E1 cells via SIRT1/p66SHC pathway and promotes osteogenesis" @default.
- W3212719347 doi "https://doi.org/10.21203/rs.3.rs-965478/v1" @default.
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