MPTP致帕金森病小鼠黑质钙结合蛋白表达变化及氯化锂对其影响

摘要

目的：观察氯化锂（LiCl）对1-甲基4-苯基-1，2，3，6四氢吡啶（MPTP）致帕金森病（PD）小鼠模型钙结合蛋白 D28K（CaBP）表达及保护作用的可能机制。方法实验小鼠随机分为正常对照（NS）组、MPTP 组、LiCl 组，采用腹腔注射 MPTP 制备模型，免疫组化与蛋白印迹技术观察中脑黑质 CaBP 表达的变化，以自主活动、滚轴、游泳实验对各组神经行为学评分。结果 MPTP 组自主活动、滚轴、游泳评分均低于正常对照组，MPTP 组 CaBP 阳性细胞数比正常对照组少，MPTP 组 CaBP 蛋白表达较对照组表达少（P<0.05）。与 MPTP 组比较，LiCl 组各行为学指标明显改善，CaBP 阳性细胞数与蛋白表达均升高（P<0.05）。结论 LiCl可增加 CaBP 的表达，减轻细胞内钙超载，是其保护 PD 损伤的机制之一。%Objective To study the expression of Calbindin-D28k and protective effect of lithium chloride on dopaminergic neurons(DA)in the substantia nigra(SN)of MPTP-induced PD mice. Method The mice were randomly divided into NS group,MPTP group,LiCl group.They were observed by behavioral paralysis agitans ratings,mobile grid number,stand number and rotarod swim test. The immunohistochemistry label the CaBP dopaminergic neurons(DA)was adopted. Western blot assay was used to determine the protein expression of CaBP in the SN of each group.Results Mobile grid number, stand number, roller experiment and swimming ability and CaBP positive neurons, protein expressions of CaBP about the MPTP group were decreased as compared with NS group(P<0.05). All the behavior score of LiCl group was improved, CaBP positive neurons, protein expressions of CaBP were increased as compared with MPTP group(P<0.05).Conclusion Lithium chloride may protect the DA neurons by regulating the expressing of CaBP, and attenuating the endocellular Ca2+ overload.