Semba J, Miyoshi R, Kito S
Division of Health Sciences, University of the Air, Chiba, Japan.
Brain Res. 1996 Oct 7;735(2):335-8. doi: 10.1016/0006-8993(96)00926-2.
To elucidate the neuroprotective effect of nicotine, we investigated whether nicotine may attenuate dexamethasone potentiation of kainic acid-induced neurotoxicity. Primary hippocampal culture was pre-treated with nicotine for 24 h followed by dexamethasone (10(-4) M) for 24 h. Then, cultures were exposed with kainic acid (10(-4) M) and cellular viability was determined by LDH effluxmetry. Nicotine pre-treatment (10(-9)-10(-7) M) dose-dependently attenuated dexamethasone potentiation of kainic acid-induced neurotoxicity. These results may support the epidemiological data suggesting a neuroprotective effect of cigarette smoking on Alzheimer's disease or Parkinson's disease.
为阐明尼古丁的神经保护作用，我们研究了尼古丁是否可减轻地塞米松对 kainic 酸诱导的神经毒性的增强作用。原代海马培养物先用尼古丁预处理 24 小时，随后用地塞米松（10(-4) M）处理 24 小时。然后，将培养物暴露于 kainic 酸（10(-4) M）中，并通过 LDH 外流量测定法测定细胞活力。尼古丁预处理（10(-9)-10(-7) M）剂量依赖性地减轻了地塞米松对 kainic 酸诱导的神经毒性的增强作用。这些结果可能支持流行病学数据，表明吸烟对阿尔茨海默病或帕金森病具有神经保护作用。
