摘要
目的研究血浆地塞米松增高后脑内细胞钙离子与阿尔茨海默病之间的关系。方法用体外观察地塞米松与脑细胞钙平衡改变之间的关系,采用Fura2/AM测定Wistar乳鼠脑细胞游离钙的方法观察地塞米松的影响。同时分别应用尼卡地平作为电压依赖性钙通道阻滞剂、氯化镁作为受体依赖性钙通道的阻滞剂,来确定地塞米松是通过何种钙通道使钙内流的。结果分别加入19μmol/L、39μmol/L地塞米松后与加入前相比,脑细胞内游离钙离子含量均明显升高(P<0.05),而加入39μmol/L地塞米松组又明显高于加入19μmol/L地塞米松组(P<0.05)。地塞米松与尼卡地平(电压依赖性钙通道阻滞剂)同时加入时,胞浆游离钙仍明显升高(P<0.05)。在地塞米松与氯化镁(受体依赖性钙通道阻滞剂)同时加入时,脑细胞胞浆游离钙离子含量均增多(P<0.05)。证实了地塞米松是通过电压依赖性钙通道和受体依赖性钙通道使钙离子流入脑细胞的。结论地塞米松可使鼠脑细胞内钙超载,后者可能与阿尔茨海默病的发生有关。
Objective To study the effect of dexamethasone acetate (DA) on [Ca 2+ ]i in brain cells in vitro so as to explore the relationship between [Ca 2+ ]i in brain cells and Alzheimer′s disease. Methods The effect of DA on brain cells [Ca 2+ ]i in sucking rats were tested with Fura 2/AM. Nikadipine (the voltage dependent calcium channel′s blockade), and Mgcl 2 (receptor dependent calcium channel′s blockade) were used to determine through what channel DA made Ca 2+ flow into brain cells. Results DA with different concentration could increased the [Ca 2+ ]i in brain cells of sucking rats ( P <0.05). And DA caused Ca 2+ to flow into brain cells through both the voltage dependent calcium channel and the receptor dependent calcium channel. Conclusion It is suggested that DA could cause the overload of Ca 2+ in brain cells, which may be linked to the development of Alzheimer′s disease.
出处
《中华精神科杂志》
CAS
CSCD
1999年第1期36-37,共2页
Chinese Journal of Psychiatry
关键词
地塞米松
痴呆
早老性痴呆
药物疗法
钙离子
Alzheimer′s disease Dexamethasone Calcium metabolism disorders Brain Rats,Wistar Disease models,animal