Zhou Liang, Kuai Feng, Shi Qin, Yang Huilin
Department of Orthopaedic Surgery, The First Affiliated Hospital of Soochow University Suzhou 215006, China.
Department of Orthopaedic Surgery, Lianshui County Hospital Huai'an 223001, China.
Am J Transl Res. 2020 Sep 15;12(9):5640-5654. eCollection 2020.
Clinical evidence suggests that doxorubicin (DOX), as a chemotherapeutic drug, can induce severe bone damage in cancer patients. However, the effect of DOX on osteoporosis has not been fully elucidated. Therefore our study aims to investigate the effect and mechanism of DOX in osteoporosis. In our study, we co-cultured rat BMSCs with different concentrations of DOX solution, then the osteogenic differentiation markers and proliferation ability were analyzed. The results indicated that a certain concentration of the DOX solution may restrain the osteogenic differentiation of rat BMSCs by bmp-2/smads signalling pathway. Also, we found DOX promoted the receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL)-induced osteoclast formation. Our research explains excellently the induce-osteoporotic mechanism of DOX in vitro, which maybe contributing to the exploration of a new way to prevent osteoporosis caused by chemotherapy.
临床证据表明，阿霉素（DOX）作为一种化疗药物，可在癌症患者中引起严重的骨损伤。然而，DOX对骨质疏松症的影响尚未完全阐明。因此，我们的研究旨在探讨DOX在骨质疏松症中的作用及机制。在我们的研究中，我们将大鼠骨髓间充质干细胞（BMSCs）与不同浓度的DOX溶液共培养，然后分析成骨分化标志物和增殖能力。结果表明，一定浓度的DOX溶液可能通过骨形态发生蛋白-2（BMP-2）/小母细胞（SMAD）信号通路抑制大鼠BMSCs的成骨分化。此外，我们发现DOX促进核因子κB（NF-κB）配体（RANKL）诱导的破骨细胞形成。我们的研究很好地解释了DOX在体外诱导骨质疏松症的机制，这可能有助于探索预防化疗引起的骨质疏松症的新方法。
