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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. hykyale@yahoo.com
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.
Abstract

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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