Institute of Chemistry and Chemical Engineering, Qiqihar University, Qiqihar 161006, People's Republic of China.
J Nat Med. 2012 Jan;66(1):25-31. doi: 10.1007/s11418-011-0545-7. Epub 2011 May 25.
Ginkgolide K, a natural platelet-activating factor receptor antagonist, was isolated from the leaves of Ginkgo biloba. However, little is known about its neuroprotective effect in ischemia-reperfusion (I/R)-induced cerebral injury. Hence, the present study was carried out to investigate the effect of ginkgolide K on neuroprotection and the potential mechanisms in the rat I/R model induced by middle cerebral artery occlusion (MCAO). The rats were pretreated with ginkgolide K 2, 4 and 8 mg/kg (i.v.) once a day for 5 days before MCAO. Neurological deficit score (NDS), brain water content, 2,3,5-triphenyltetrazolium chloride (TTC) staining and pathology of brain tissue, as well as indexes of oxidative stress [superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO) and nitric oxide synthase (NOS)] were measured at 24 h after ischemia. The results indicated that pretreatment with ginkgolide K significantly diminished the volume of infarction and brain water content, and improved NDS. Moreover, ginkgolide K markedly reversed the level of MDA, NO, NOS and SOD to their normal state in serum or cerebral ischemic section. In addition, hematoxylin and eosin staining showed the neuronal injury was significantly improved after being pretreated with ginkgolide K. These findings demonstrate that ginkgolide K exhibits neuroprotective properties through its antioxidative action in MCAO rats.
银杏内酯 K 是一种天然血小板激活因子受体拮抗剂，从银杏叶中分离得到。然而，关于其在缺血再灌注（I/R）诱导的脑损伤中的神经保护作用知之甚少。因此，本研究旨在探讨银杏内酯 K 在大脑中动脉闭塞（MCAO）诱导的大鼠 I/R 模型中的神经保护作用及其潜在机制。大鼠在 MCAO 前每天静脉注射银杏内酯 K 2、4 和 8mg/kg（一次），预处理 5 天。在缺血后 24 小时测量神经功能缺损评分（NDS）、脑含水量、2,3,5-三苯基氯化四氮唑（TTC）染色和脑组织病理学以及氧化应激指标[超氧化物歧化酶（SOD）、丙二醛（MDA）、一氧化氮（NO）和一氧化氮合酶（NOS）]。结果表明，银杏内酯 K 预处理显著减少了梗死体积和脑含水量，改善了 NDS。此外，银杏内酯 K 明显将 MDA、NO、NOS 和 SOD 的水平恢复到血清或脑缺血部位的正常状态。此外，苏木精和伊红染色显示，银杏内酯 K 预处理后神经元损伤明显改善。这些发现表明，银杏内酯 K 通过其在 MCAO 大鼠中的抗氧化作用发挥神经保护作用。
