Apoptosis of bone marrow-derived mesenchymal stem cells (BM-MSCs) has been shown to contribute to the development of osteoporosis, which is often the result of long-term use of glucocorticoid drugs such as dexamethasone (Dex). However, it remains unknown whether Dex induces apoptosis of BM-MSCs, and whether a chemical agent like vanadate can block such effects. To investigate these two issues, we isolated BM-MSCs from SD rats and treated the cells with different doses of Dex. We found that Dex induced apoptosis in dose- and time-dependent manners. Pretreating BM-MSCs with vanadate prevented Dex-induced apoptosis. Furthermore, we found that expression of caspases (3, 8, and 9) increased in Dex-treated BM-MSC and was attenuated by vanadate pretreatment. These results not only demonstrate the role of vanadate in the inhibition of Dex-induced apoptosis of BM-MSCs, but also reveal the therapeutic potential of vanadate in glucocorticoid-mediated osteoporosis.

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