摘要
目的 探索胶质瘤性脑水肿的病理生理变化及其分子机制。方法 利用体外血 -脑脊液屏障模型研究胶质瘤细胞对血 -脑脊液屏障水转运的影响。采用半定量 RT-PCR方法分析胶质瘤细胞作用后体外血 -脑脊液屏障模型胶质细胞水通道 4( AQP4)的表达变化。结果 胶质瘤细胞可明显增强体外血 -脑脊液屏障模型对水由内皮细胞腔面向基底面的扩散 ,这一过程不依赖于清蛋白等大分子物质的通透性变化。同时 ,胶质瘤细胞明显降低了胶质细胞 AQP4的表达水平。结论 胶质瘤细胞可明显增强体外血 -脑脊液屏障模型对水由内皮细胞腔面向基底面的扩散。胶质瘤性脑水肿不一定是血浆等大分子物质通透性增加的结果。胶质瘤细胞对胶质细胞
Objective To investigate the mechanism of brain edema induced by glioma cells. Methods The change of water transport of in vitro blood brain barrier model was determined by HPLC. The expression level of aquaporin 4(AQP4) was analyzed by semiquatitative RT PCR. Results The water transport of in vitro blood CSF barrier model from luminal side to abluminal side was promoted after coculture with glioma cells. The expression level of AQP4 of astrocytes was decreased dramatically by the influence of glioma cells. Conclusions Glioma cells can increase the water transport of in vitro blood CSF barrier model from luminal side to abluminal side. The edema induced by glioma cells may not be the result of hyperpermeability of blood CSF barrier to macromolecules in plasma. The decreased expression level of AQP4 induced by glioma cells is suggested to be a molecular mechanism of neoplastic brain edema in glioma patients.
出处
《中国神经免疫学和神经病学杂志》
CAS
2004年第5期300-303,共4页
Chinese Journal of Neuroimmunology and Neurology
基金
国家自然科学基金资助项目 (3 0 17961)
军队"十五"重点项目基金资助项目(0 1ZD5 4)
