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目的 :研究刺尾鱼毒素 (maitotoxin ,MTX)对神经胶质瘤细胞 (NG10 8)毒性作用机制 ,为探讨可能的防治途径提供理论依据。方法 :采用噻唑蓝 (MTT)比色法检测MTX对细胞的毒性。结果 :NG10 8细胞对MTX的作用比较敏感。MTX作用 4h内细胞存活率明显呈剂量、时间依赖性下降 ;毒素作用 1h的LD50 值为 0 .5 3ng/ml。MTX的细胞毒性与胞外Ca2 + 浓度关系密切 ,随着胞外Ca2 + 的升高 ,MTX的毒性增大 ,胞外无Ca2 + 时 ,观察不到MTX对NG10 8细胞的毒性作用。硝苯地平可以明显抑制MTX的细胞毒性。结论 :MTX是一种作用强烈的生物毒素 ,它对NG10 8细胞的毒性效应与胞内Ca2 + 超载有关 ,Ca2 + 通道阻断剂硝苯地平可在一定程度上抑制MTX的毒性效应。
Objective: To study the mechanism of cytotoxicity of maitotoxin (MTX) on glioma cells (NG10 8), and to provide a theoretical basis for exploring possible prevention and cure ways. Methods: Toxicity of MTX to cells was detected by MTT assay. Results: NG108 cells were more sensitive to MTX. The cell viability in MTX treated group was significantly decreased in a dose-and time-dependent manner within 4 hours. The LD50 value of toxin-treated cells for 1 hour was 0.53 ng / ml. The cytotoxicity of MTX was closely related to the concentration of extracellular Ca2 +. With the increase of extracellular Ca2 +, the cytotoxicity of MTX increased and no cytotoxicity of MTX on NG108 cells was observed when extracellular Ca2 + was absent. Nifedipine significantly inhibited MTX cytotoxicity. CONCLUSION: MTX is a potent biotoxin, and its toxic effect on NG108 cells is related to intracellular Ca2 + overload. Ca2 + channel blocker nifedipine can inhibit the toxic effect of MTX to a certain extent.