Department of Zoology, Faculty of Science, Alexandria University, Alexandria, Egypt.
Faculty of Art and Science- Badr, Al-Jabal Al-Gharbi University, Gherian, Libya.
Curr Pharm Biotechnol. 2020;21(12):1259-1268. doi: 10.2174/1389201021666200320135849.
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.
The current study aimed to investigate the neuroprotective effect of GbE in a rat model of PD induced by rotenone (ROT; a neurotoxin).
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.
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.
GbE mitigated ROT-induced PD via the inhibition of free-radical production, scavenging of ROS, and antioxidant enhancement.
银杏叶提取物（GbE）含有多种生物活性化合物，具有自由基清除活性。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丧失，并与氧化应激、神经炎症和细胞凋亡有关。
本研究旨在探讨银杏叶提取物（GbE）对鱼藤酮（ROT；神经毒素）诱导的 PD 大鼠模型的神经保护作用。
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。
口服 ROT（2.5mg/kg b.w.）50 天导致大脑中脂质过氧化产物生成增加，还原型谷胱甘肽、总巯基含量和超氧化物歧化酶和谷胱甘肽过氧化物酶等酶抗氧化剂活性显著降低。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升高，纹状体和黑质中的多巴胺显著降低。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 治疗（150mg/kg b.w./天）可显著降低升高的氧化应激标志物和促炎细胞因子，并恢复降低的抗氧化酶活性、DA 水平和 TH 表达。这些结果通过组织学观察得到证实，清楚地表明 GbE 对 ROT 诱导的 PD 具有神经保护作用。
GbE 通过抑制自由基产生、清除 ROS 和增强抗氧化作用来减轻 ROT 诱导的 PD。
