National Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing, China.
Biol Pharm Bull. 2011;34(8):1291-6. doi: 10.1248/bpb.34.1291.
In the present study, we investigated the neuroprotective effects of kaempferol in the mouse model of Parkinson's disease, which was induced by neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). We confirmed that MPTP led to behavioral deficits, depletion of dopamine and its metabolites, reduction in superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activity, and the elevation of malondialdehyde (MDA) levels in the substantia nigra. When administered prior to MPTP, kaempferol improved motor coordination, raised striatal dopamine and its metabolite levels, increased SOD and GSH-PX activity, and reduced the content of MDA compared with mice treated with MPTP alone. Immunohistochemical studies using anti-tyrosine hydroxylase (TH) antibody showed that medication of kaempferol could prevent the loss of TH-positive neurons induced by MPTP. Taken together, we propose that kaempferol has shown anti-parkinsonian properties in our studies. More work is needed to explore detailed mechanisms of action.
在本研究中，我们研究了山奈酚在神经毒素 1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的帕金森病小鼠模型中的神经保护作用。我们证实 MPTP 导致行为缺陷、多巴胺及其代谢物耗竭、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-PX）活性降低以及黑质中丙二醛（MDA）水平升高。当在 MPTP 之前给予山奈酚时，与单独用 MPTP 治疗的小鼠相比，山奈酚改善了运动协调能力，提高了纹状体多巴胺及其代谢物水平，增加了 SOD 和 GSH-PX 活性，并降低了 MDA 的含量。使用抗酪氨酸羟化酶（TH）抗体的免疫组织化学研究表明，山奈酚的给药可以预防 MPTP 诱导的 TH 阳性神经元的丢失。综上所述，我们提出山奈酚在我们的研究中表现出抗帕金森病的特性。需要进一步的工作来探索其作用机制的详细信息。
