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首页> 外文期刊>The Canadian Journal of Neurological Sciences: le Journal Canadien des Sciences Neurologiques >Effects of Ginkgo Biloba Extract on A53T α-Synuclein Transgenic Mouse Models of Parkinson’s Disease
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Effects of Ginkgo Biloba Extract on A53T α-Synuclein Transgenic Mouse Models of Parkinson’s Disease

机译：Ginkgo Biloba提取物对帕金森病的A53Tα-突触核蛋白转基因小鼠模型的影响

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Background: Parkinson’s disease (PD) is a degenerative disorder of the central nervous system mainly affecting the motor system. Presently, there is no effective and safe drug to treat patients with PD. Ginkgo biloba extract (GBE), obtained from leaves of the Ginkgo biloba tree, is a complex mixture of ingredients primarily containing two active components: flavonoids and terpenoids. In this study, we investigated the effects of GBE on A53T α-synuclein transgenic mice, a PD model that has better simulated the progression of PD patients than other models such as the 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine–induced PD model. Methods: Fifty α-synuclein A53T transgenic mice were fed and treated with GBE, and locomotor activity was detected by pole test, forced swim test, and wire-hang test. The expression of tyrosine hydroxylase and dopamine transporters was detected using immunohistochemistry. Superoxide dismutase activity, glutathione peroxidase activity, and malondialdehyde expression were detected using an assay kit. Results: Our results show that GBE treatment improved locomotor activity and that superoxide dismutase and glutathione peroxidase inhibited the expression of methane dicarboxylic aldehyde and recovered the expression of tyrosine hydroxylase and dopamine transporters. Conclusions: The GBE treatment improved locomotor activity and inhibited the development of PD in the A53T α-synuclein transgenic mice, which may be partly responsible for decreased oxidative damage and maintain the normal dopamine homeostasis.
机译：背景：帕金森病（PD）是主要影响电机系统的中枢神经系统的退行性障碍。目前，没有有效和安全的药物治疗PD患者。从银杏树的叶片获得的银杏叶（GBE）是一种复杂的成分混合物，主要包含两个活性成分：黄酮类化合物和三萜类化合物。在这项研究中，我们研究了GBE对A53Tα-突触核蛋白转基因小鼠的影响，PD模型更好地模拟PD患者的进展，而不是如1-甲基-4-苯基-1,2,3， 6四氢吡啶诱导的PD模型。方法：用GBE喂养并用GBE处理和处理50α-突触核蛋白，并通过极值试验，强制游泳试验和线挂测试检测运动活性。使用免疫组织化学检测酪氨酸羟化酶和多巴胺转运蛋白的表达。使用测定试剂盒检测超氧化物歧化酶活性，谷胱甘肽过氧化物酶活性和丙二醛表达。结果：我们的研究结果表明，GBE治疗改善了运动活性，超氧化物歧化酶和谷胱甘肽过氧化物酶抑制甲烷二羧酸醛的表达，回收酪氨酸羟化酶和多巴胺转运蛋白的表达。结论：GBE治疗改善了运动活性并抑制A53Tα-突触核蛋白转基因小鼠中Pd的发育，这部分原因是降低氧化损伤并维持正常的多巴胺稳态。

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