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桃叶珊瑚苷可减轻1-甲基-4-苯基-1,2,3,6-四氢吡啶诱导的帕金森病小鼠的神经胶质细胞活化并保护多巴胺能神经元。

Aucubin alleviates glial cell activation and preserves dopaminergic neurons in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced parkinsonian mice.

作者信息

Zhu Ying-Li, Sun Meng-Fei, Jia Xue-Bing, Zhang Pei-Hao, Xu Yi-Da, Zhou Zhi-Lan, Xu Zhou-Heng, Cui Chun, Chen Xue, Yang Xu-Sheng, Shen Yan-Qin

机构信息

Wuxi Medical School, Jiangnan University.

Wuxi People's Hospital, Wuxi, China.

出版信息

Neuroreport. 2018 Sep 5;29(13):1075-1083. doi: 10.1097/WNR.0000000000001075.

DOI:10.1097/WNR.0000000000001075
PMID:29985188
Abstract

Aucubin (AUC) is a major bioactive ingredient in Eucommia ulmoides, Plantain asiatica, and Aucuba japonica, and has been shown to exert anti-inflammatory, antioxidative, and neuroprotective effects. We explore the neuroprotective effects of AUC in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonian mice. Mice were administered MPTP (30 mg/kg) daily for 5 days, followed by treatment with AUC for 7 days. Measurement of dopamine levels was performed by high-performance liquid chromatography and tyrosine hydroxylase expression was assessed by western blot. Our results showed that AUC treatment improved mobility in the pole descent test and the traction test, and reduced the loss of dopaminergic neurons in MPTP-induced parkinsonian mice. AUC treatment rescued the decreased dopamine and tyrosine hydroxylase levels in the striatum of parkinsonian mice. Furthermore, AUC treatment reduced both microglia and astrocyte activation in the substantia nigra of parkinsonian mice. These findings suggest that AUC exerts neuroprotective effects, in part by reducing inflammation and preserving dopaminergic neurons. Possible protection mechanisms involved in MPTP-induced parkinsonian mice need to be clarified further.

摘要

桃叶珊瑚苷(AUC)是杜仲、车前草和东瀛珊瑚中的主要生物活性成分,已被证明具有抗炎、抗氧化和神经保护作用。我们探究了AUC对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的帕金森病小鼠的神经保护作用。小鼠连续5天每天给予MPTP(30mg/kg),随后用AUC治疗7天。通过高效液相色谱法测定多巴胺水平,通过蛋白质免疫印迹法评估酪氨酸羟化酶的表达。我们的结果表明,AUC治疗改善了小鼠在杆下降试验和牵引试验中的运动能力,并减少了MPTP诱导的帕金森病小鼠中多巴胺能神经元的损失。AUC治疗挽救了帕金森病小鼠纹状体中多巴胺和酪氨酸羟化酶水平的降低。此外,AUC治疗减少了帕金森病小鼠黑质中小胶质细胞和星形胶质细胞的活化。这些发现表明,AUC发挥神经保护作用,部分是通过减轻炎症和保护多巴胺能神经元。MPTP诱导的帕金森病小鼠中可能的保护机制需要进一步阐明。

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