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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Selegiline potentiates the effects of EGb 761 in response to ischemic brain injury.
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Selegiline potentiates the effects of EGb 761 in response to ischemic brain injury.

机译：司来吉兰可增强EGb 761对缺血性脑损伤的反应。

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摘要

We evaluated whether combined treatment with selegiline, a selective MAO-B inhibitor, and EGb 761, a standard extract of Ginkgo biloba, has synergistic effects against ischemic reperfusion injury (IRI) in gerbils. Interestingly, we observed that pretreatment with EGb 761 significantly attenuated selegiline-induced hyperactivity. This finding paralleled striatal fos-related antigen immunoreactivity (FRA-IR) in mice. Four minutes of bilateral carotid artery occlusion caused substantial cell loss in the CA1 of the hippocampus 5 days post-ischemic insult. Pretreatment with EGb 761, with or without selegiline, significantly attenuated this neuronal loss. Combined treatment with EGb 761 plus selegiline was more efficacious in preventing this loss. Synaptosomal formations of protein carbonyl, lipid peroxidation (malondialdehyde (MDA) + 4-hydroxyalkenal (4-HDA)), and reactive oxygen species (ROS) in the hippocampus remained elevated 5 days post-ischemic insult. The antioxidant effects appeared to be most significant in the group treated with EGb 761 plus selegiline. This combined treatment produced more significant attenuation of IRI-induced alterations in intramitochondrial calcium accumulation, the mitochondrial transmembrane potential, and mitochondrial Mn-superoxide dismutase-like immunoreactivity (Mn-SOD-IR) than either treatment alone. Our results suggest that co-administration of EGb 761 and selegiline produces significant neuroprotective effects via suppression of oxidative stress and mitochondrial dysfunction without affecting neurological function.
机译：我们评估了与司来吉兰（一种选择性的MAO-B抑制剂）和银杏叶标准提取物EGb 761的联合治疗是否对沙鼠的缺血再灌注损伤（IRI）有协同作用。有趣的是，我们观察到用EGb 761进行的预处理显着减弱了司来吉兰诱导的过度活跃。这一发现与小鼠纹状体fos相关抗原免疫反应性（FRA-IR）相似。缺血性损伤后5天，四分钟的双侧颈动脉闭塞导致海马CA1大量细胞丢失。用EGb 761预处理（有或没有司来吉兰）可显着减轻这种神经元丢失。 EGb 761加司来吉兰的联合治疗在预防这种损失方面更为有效。缺血性损伤后5天，海马中的羰基蛋白，脂质过氧化（丙二醛（MDA）+ 4-羟基烯醛（4-HDA））和活性氧（ROS）的突触体形成仍然升高。在用EGb 761加司来吉兰治疗的组中，抗氧化作用似乎最为明显。与单独的任何一种治疗相比，这种联合治疗对IRI诱导的线粒体内钙积累，线粒体跨膜电位和线粒体Mn超氧化物歧化酶样免疫反应性（Mn-SOD-IR）的改变的抑制作用更为显着。我们的结果表明，EGb 761和司来吉兰的共同给药可通过抑制氧化应激和线粒体功能障碍而产生显着的神经保护作用，而不会影响神经功能。

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