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作 者:杜静[1] 单璐琛[1] 张高小[1] 王玉强[1]
机构地区:[1]暨南大学药学院新药研究所,广东广州510632
出 处:《时珍国医国药》2011年第7期1564-1565,共2页Lishizhen Medicine and Materia Medica Research
基 金:国家自然科学基金(No.30973618);国家重大新药创制(No.2009ZX09103-031)
摘 要:目的观察川芎嗪体外、体内对MPTP导致的多巴胺能(dopaminergic,DA)神经元毒性的影响。方法体外实验,提取孕14 d的Sprague-dawley大鼠胎鼠黑质区多巴胺神经元,MPP+诱导其损伤,运用免疫荧光法测定黑质酪氨酸羟化酶(tyrosine hydroxylase,TH)阳性神经元数量及状态变化;体内实验,以C57BL/6J小鼠为研究对象,采用腹腔注射MPTP方法制作小鼠慢性帕金森(Parkinson's disease,PD)模型,运用免疫组化法测定TH阳性神经元数量变化。结果体外实验:TMP组多巴胺神经元形态数目均有所改善,其中500μmol/L组与模型组相比具显著性差异。体内实验:与模型组相比,注射TMP后,多巴胺神经元密度有所增加。结论 TMP能不同程度地改善MPTP诱导的多巴胺神经元的损伤。ObjectiveTo investigate the effect of tetramethylpyrazine(TMP) on dopaminergic neuron injury induced by N-methyl-4-phenyl-1,2,3,6-tetrahydro-pyridine(MPTP) in vitro and in vivo.MethodsIn vitro: Rat mesencephalic neurons were cultured for 5 days,followed by addition of MPP+.The number and morphology of positive TH neurons were observed using an inverted fluorescence microscope.In vivo: Mice were administered MPTP(25 mg/kg,i.p,per day) for 5 days to establish the PD animal model.The number of positive TH cells in the SNpc was observed by immunohistochemistry.ResultsIn vitro: The number of dopaminergic neurons and the neurite length in the TMP group were increased compared to that of the MPP+ group.In vivo,TMP treatment increased the density of dopaminergic neuron injury induced by MPTP.ConclusionTMP can protect dopaminergic neuron injured by MPP+ and is beneficial in MPTP-induced PD animal model.
分 类 号:R245.3[医药卫生—针灸推拿学]
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