摘要
目的:观察诱导型一氧化氮合酶(iNOS)特异性抑制剂氨基胍(AG)对帕金森病模型小鼠黑质内多巴胺(DA)能神经元的影响。方法:采用Lau法制作PD小鼠模型,通过行为学观察和免疫印迹法,观察PD小鼠模型的行为学表现,及腹侧中脑(包括VTA和SN)iNOS、酪氨酸羟化酶(TH)表达水平的变化。并观察给予iNOS抑制剂AG后对上述变化的影响。结果:与对照小鼠相比,PD小鼠出现PD典型的行为学表现,腹侧中脑TH含量下降约77%,同时i-NOS含量大幅度升高。经iNOS抑制剂AG处理的PD小鼠行为表现明显减轻,腹侧中脑TH含量仅下降约41%,腹侧中脑iNOS含量也较模型组明显为低。结论:iNOS的表达与PD模型小鼠黑质内DA能神经元的丢失有关;AG可能对PD模型小鼠黑质内DA能神经元有保护作用。
Objective： To observe the effect of aminoguanidine （AG）, the specific inhibitor of induced nitricoxide synthase （iNOS）,on the DA neurons of the Parkinson＇s disease model mice. Mothods： To make the model mice of PD by lan method. To observe the behavior of the PD mice by the behavioral science and the expression of the iNOS and TH in the gastro-midbrain by western blot, further observe the changes when AG was added. Results： Compared with the control group, the typical performance appeared in the PD model mice, the content of TH in the gastro-midbrain decreased about seventy-seven percent, at the same time, the content of iNOS increased dramatically. Compared with the control group, the behavior of PD mice treated with AG alleviate extremely ,the content of TH decreased about forty-four percent, the content of iNOS was also much lower than that of the control group. Conclusion： The loss of DA neurons in the substantia nigra has correlation with the expression of iNOS, maybe AG can protect the DA neurons.
出处
《中国医药导报》
CAS
2007年第12X期17-18,共2页
China Medical Herald
作者简介
师亮：通讯作者，山西医科大学组织胚胎学教研室。
