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J Korean Soc Osteoporos. 2010 Aug;8(2):171-177. Korean. Original Article.
Jung MH , Lee TH , Oh YL , Lee JY , Yang SO , Choi WH , Kim HY .
Department of Obstetrics and Gynecology, Kyung Hee University, Seoul, Korea.
Department of Obstetrics and Gynecology, Kosin University, Busan, Korea.
Department of Obstetrics and Gynecology, Konkuk University, Seoul, Korea.
Department of Radiology, Asia Cancer Center, Busan, Korea.
Department of Internal Medicine, Hanyang University, Seoul, Korea.

OBJECTIVES: This study examined the ability of Cyclosporine (CsA) to induce apoptosis in a rat osteoblast cell line. METHODS: Rat osteoblast ROS 17/2.8 cells were cultured, and treated with with 0.1~40 microg/mL CsA for 24 hours after plating of cells. Cell viability was determined by the MTT assay. Western Blot Analysis was done with primary antibodies to caspase-3 and caspase-8. Reactive oxygen species (ROS) synthesis was measured by flowcytometry. RESULTS: Cell viability decreased in dose-dependent manner with increasing concentrations of CsA. Treatment of ROS 17/2.8 cells with 0.1, 0.5, 1, 5, 10, 20, or 40 microg/mLg/mL CsA caused 85%, 80%, 73%, 60%, 45%, 40%, and 27% cell viability, respectively. Western blot analysis showed reduced caspase-3 expression and induced caspase-8. The ROS in a dose-and time-dependent manner were increased by CsA. CONCLUSION: These results suggest that CsA can induce oxygen free radicals which appears to trigger apoptosis by activating pro-apoptotic signals. CsA plays a role in the post-transplatation bone diseases via the induction of apoptosis in osteoblast.

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