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首页> 外文期刊>Nutrients >Pycnogenol ? Supplementation Attenuates Memory Deficits and Protects Hippocampal CA1 Pyramidal Neurons via Antioxidative Role in a Gerbil Model of Transient Forebrain Ischemia
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Pycnogenol ? Supplementation Attenuates Memory Deficits and Protects Hippocampal CA1 Pyramidal Neurons via Antioxidative Role in a Gerbil Model of Transient Forebrain Ischemia

机译:pycnogenol?补充通过在短暂的前脑缺血的Gerbil模型中通过抗氧化作用衰减记忆缺陷并保护海马CA1金字塔神经元

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Pycnogenol ? (an extract of the bark of French maritime pine tree) is used for dietary supplement and known to have excellent antioxidative efficacy. However, there are few reports on neuroprotective effect of Pycnogenol ? supplementation and its mechanisms against ischemic injury following transient forebrain ischemia (TFI) in gerbils. Now, we examined neuroprotective effect and its mechanisms of Pycnogenol ? in the gerbils with 5-min TFI, which evokes a significant death (loss) of pyramidal cells located in the cornu ammonis (CA1) region of gerbil hippocampus from 4–5 days post-TFI. Gerbils were pretreated with 30, 40, and 50 mg/kg of Pycnogenol ? once a day for 7 days before TFI surgery. Treatment with 50 mg/kg, not 30 or 40 mg/kg, of Pycnogenol ? potently protected learning and memory, as well as CA1 pyramidal cells, from ischemic injury. Treatment with 50 mg/kg Pycnogenol ? significantly enhanced immunoreactivity of antioxidant enzymes (superoxide dismutases and catalase) in the pyramidal cells before and after TFI induction. Furthermore, the treatment significantly reduced the generation of superoxide anion, ribonucleic acid oxidation and lipid peroxidation in the pyramidal cells. Moreover, interestingly, its neuroprotective effect was abolished by administration of sodium azide (a potent inhibitor of SODs and catalase activities). Taken together, current results clearly indicate that Pycnogenol ? supplementation can prevent neurons from ischemic stroke through its potent antioxidative role.
机译:pycnogenol? (法国海洋松树的树皮提取物)用于膳食补充剂,并已知具有优异的抗氧化疗效。然而,少含有关于Pycnogenol的神经保护作用的报道?在Gerbils中瞬态前脑缺血(TFI)后缺血性损伤的补充及其机制。现在,我们检查了神经保护作用及其碧萝芷机制?在患有5分钟的TFI中,引起了位于TFI后4-5天的Gerbil Hippocampus的Cornu Ammonis(CA1)区的锥形细胞的显着死亡(丧失)。用30,40和50mg / kg的碧萝芷预处理辣椒?在TFI手术前每天持续7天。用50mg / kg,而不是30或40mg / kg的pycnogen治疗?从缺血性损伤,缺血性损伤以及Ca1金字塔孔细胞的易受保护的学习和记忆。用50mg / kg碧萝芷治疗? TFI诱导前后金字塔细胞中抗氧化酶(超氧化物脱粉酶和过氧化氢酶)显着增强了免疫反应性。此外,治疗显着降低了锥体细胞中超氧化物阴离子,核糖核酸氧化和脂质过氧化的产生。此外,有趣的是,通过施用叠氮化钠(一种SODS和过氧化氢酶活酶活性)废除其神经保护作用。一起服用,目前的结果清楚地表明碧萝芷?补充可以通过其有效的抗氧化作用预防神经元来自缺血性卒中。

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