摘要
目的:探讨硫酸化茯苓多糖(SP)对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导小鼠黑质多巴胺(DA)能神经元的保护作用。方法:ICR小鼠随机分为5组:对照组、MPTP模型组和SP治疗组(50、100、150 mg/kg),实施腹腔注射给药。爬杆行为评价各组小鼠的运动能力,酪氨酸羟化酶(TH)免疫染色法和TUNEL法检测黑质神经元的损伤与凋亡情况,紫外分光光度法检测小鼠中脑和纹状体中DA含量、纹状体中一氧化氮合酶(NOS)活性。结果:MPTP组中小鼠的爬杆时间显著延长,TH阳性细胞明显减少,TUNEL阳性细胞数量增加,中脑和纹状体中的多巴胺含量显著下降(P<0.01),纹状体中NOS活性显著上升(P<0.01)。SP治疗组中,MPTP导致的上述变化均得到改善:小鼠爬杆时间缩短,TH阳性细胞增多,TUNEL阳性细胞减少;小鼠中脑和纹状体DA含量显著上升(P<0.01),NOS活性明显下降(P<0.05)。结论:SP对MPTP诱导的帕金森小鼠黑质DA能神经元具有一定的保护作用。
AIM： To explore the protective effect of sulfated pachymaran （SP） on MPTP- in- duced damage in mouse substantia nigra neurons. METHODS： ICR mice were randomly divided into five groups： control group, MPTP model group and SP group （50, 100, 150 mg/kg）, and all drugs were administrated to mice by abdominal injection. Pole test was performed to assess the ability of mov- ing. TH immunostaining and TUNEL labeling were used to observe the damage and apoptosis of nigral neurons. The levels of dopamine （DA） , malondial- dehvde （MDA） and hydrogen peroxide （ H2O2 ） in both midbrain and striatum were detected by UV spectrophotometry. RESULTS： Compared with the control group, the mice in MPTP model group took longer time to descend; TH-positive neurons and the level of DA in midbrain and striatum decreased obvi- ously, and TUNEL-positive neurons increased signif- icantly, but the level of He 02 in midbrain and stria- turn did not vary significantly. Compared with the model group, SP treatment was shown to reverse all the above changes induced by MPTP. CONCLUSION： SP may have protective effects on MPTP-induced damage of dopaminergic neurons in Parkin- sons＇ disease PD mice
出处
《中国临床药理学与治疗学》
CAS
CSCD
2017年第1期37-42,共6页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
安徽省教育厅自然科学基金资助项目(KJ2013A242)
国家自然科学基金资助项目(31400307)
宿州学院博士启动基金项目(2014jb05)
