盐酸埃他卡林对H2O2所致PC12细胞损伤的保护

目的: 研究 K_ATP 通道开放剂盐酸埃他卡林(iptakalim hydrochloride, Ipt) 对 H₂O₂ 所致 PC12 细胞损伤的保护作用及其作用机制。方法: 采用培养的PC12细胞, MTT 法测定细胞存活率, HPLC 法测定细胞培养液中谷氨酸(Glu) 的含量, 荧光法测定胞内钙离子(Ca²⁺]_i) 浓度。结果: Ipt 可浓度依赖性的拮抗H₂O₂ 介导的细胞毒性, 提高细胞生存率, 降低胞外Glu的释放以及胞内 Ca²⁺ 浓度。该保护作用可被200 μmol°L^-1 5-HD(线粒体K ATP 通道阻断剂) 部分拮抗。结论: Ipt 可拮抗 H₂O₂ 介导的细胞损伤作用, 该保护作用可能与线粒体ATP 敏感性钾通道相关。

Effects of iptakalim hydrochloride on H2O2 induced cytotoxicity in pheochromocytoma(PC12) cells

AIM: To investigate the protective effects and mechanisms of iptakalim hydrochloride(Ipt) on H₂O₂ induced neurotoxity. METHODS: Neurotoxity injury was induced by H₂O₂ in PC12 cells.The cell viability was tested by MTT assay. The glutamate released from PC12 cells was measured by HPLC combined with fluorescent detector analysis.Changes in the intracellular free Ca²⁺ concentration (Ca²⁺]_i) were determined in fluo-3 AM loaded PC12 cells.RESULTS: Ipt (1, 10 and 100μmol°L^-1) markedly mitigated H₂O₂ -induced neurotoxi-ty, 10μmol°L^-1 Ipt inhibited the release of glutamate and the increase of (Ca²⁺]_i) induced by H₂O₂. The pro-tective effectswas incompletely blocked by 5-HDwhich is a mitochondrial K ATP channels antagnist. CONCLUSION: Ipt provides neuroprotective effects on H₂O₂ in-duced cytoxixity in cultured PC12 cells and the protective effects may be partially related with mitochondrial KATP channels.