백서 조골세포주에서의 싸이클로스포린 산소유리기 유도능
The Ability of Cyclosporine (CsA) to Induce Oxigen Free Radicals in a Rat Osteoblast Cell Line
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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 0.1～40μg/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 μg/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.
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 0.1～40μg/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 μg/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.
참고문헌 (38)
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