Background: Ginkgo biloba extract (GbE) is known to contain several bioactive compounds and exhibits free radical scavenging activity. Parkinson's Disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons and is associated with oxidative stress, neuroinflammation and apoptosis.

Objective: The current study aimed to investigate the neuroprotective effect of GbE in a rat model of PD induced by rotenone (ROT; a neurotoxin).

Methods: Twenty-four male albino rats were randomly divided into four groups of six rats each: normal control, GbE treated, toxin control (ROT treated) and GbE+ROT group.

Results: Oral administration of ROT (2.5 mg/kg b.w.) for 50 days caused an increased generation of lipid peroxidation products and significant depletion of reduced glutathione, total thiol content and activities of enzymatic antioxidants, i.e., superoxide dismutase and glutathione peroxidase in the brains of treated rats. Furthermore, ROT caused an elevation in acetylcholinesterase, interleukin-1β, interleukin- 6 and tumor necrosis factor-α and a significant reduction in dopamine in the stratum and substantia nigra. Immunohistochemical results illustrated that ROT treatment reduced the expression of tyrosine hydroxylase (TH). GbE treatment (150 mg/kg b.w./day) significantly reduced the elevated oxidative stress markers and proinflammatory cytokines and restored the reduced antioxidant enzyme activities, DA level and TH expression. These results were confirmed by histological observations that clearly indicated a neuroprotective effect of GbE against ROT-induced PD.

Conclusion: GbE mitigated ROT-induced PD via the inhibition of free-radical production, scavenging of ROS, and antioxidant enhancement.

背景：已知银杏叶提取物 (GbE) 含有多种生物活性化合物，并具有清除自由基的活性。帕金森病 (PD) 是一种神经退行性疾病，其特征是多巴胺能神经元的丢失，并与氧化应激、神经炎症和细胞凋亡有关。

目的：本研究旨在研究 GbE 在鱼藤酮（ROT；一种神经毒素）诱导的 PD 大鼠模型中的神经保护作用。

方法：将 24 只雄性白化大鼠随机分为四组，每组 6 只：正常对照组、GbE 治疗组、毒素对照组（ROT 治疗组）和 GbE+ROT 组。

结果：连续 50 天口服 ROT（2.5 mg/kg bw）导致脂质过氧化产物的产生增加，并显着减少还原型谷胱甘肽、总硫醇含量和酶抗氧化剂的活性，即大脑中的超氧化物歧化酶和谷胱甘肽过氧化物酶治疗大鼠。此外，ROT 导致乙酰胆碱酯酶、白细胞介素-1β、白细胞介素-6 和肿瘤坏死因子-α 的升高以及黑质层和黑质中多巴胺的显着减少。免疫组织化学结果表明，ROT 处理降低了酪氨酸羟化酶 (TH) 的表达。GbE 处理（150 毫克/千克体重/天）显着降低了升高的氧化应激标记物和促炎细胞因子，并恢复了降低的抗氧化酶活性、DA 水平和 TH 表达。

结论：GbE 通过抑制自由基产生、清除 ROS 和增强抗氧化来减轻 ROT 诱导的 PD。