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Asiatic acid prevents the quinolinic acid-induced oxidative stress and cognitive impairment

机译:亚洲酸可防止喹啉酸诱导的氧化应激和认知障碍

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摘要

Increased accumulation of endogenous neurotoxin quinolinic acid has been found in various neurodegenerative diseases. Oxidative stress caused by quinolinic acid is considered as imperative factor for its toxicity. Asiatic acid, a natural triterpene is widely studied for its various medicinal values. In the present study the effects of asiatic acid in preventing the cognitive impairment and oxidative stress caused by quinolinic acid was investigated. Male Spraque-Dawley rats were orally administered asiatic acid (30 mg/kg/day) for 28 days, while quinolinic acid toxicity-induced animals received quinolinic acid (1.5 mmol/kg/day) from day 15 to day 28 for 14 days. Asiatic acid administration prevented the loss of spatial memory caused due to quinolinic acid-induced toxicity as determined using the novel object location test. In addition, asiatic acid administration alleviated the deleterious effect of quinolinic acid in brain such as increased oxidative stress, decreased antioxidant status and mitochondrial oxidative phosphorylation dysfunction. These data demonstrate that asiatic acid through its potent antioxidant and cognition enhancement property prevented the neuronal impairments caused by quinolinic acid.
机译:在各种神经变性疾病中发现了内源性神经毒素喹啉酸的增加。由喹啉酸引起的氧化应激被认为是其毒性的势不指。亚乙酸,自然三萜广泛研究其各种药物值。在本研究中,研究了亚洲酸对预防喹啉酸引起的认知损伤和氧化应激的影响。男性Spraque-Dawley大鼠口服亚氨酸(30mg / kg /天)28天,而喹啉酸毒性诱导的动物从第15天到第28天的喹啉酸(1.5mmol / kg /天)持续14天。亚肝酸给药阻止由于喹啉酸诱导的毒性引起的空间记忆损失,如使用新的物体位置测试所确定的。此外,亚洲酸给药减轻了血液酸在脑中的有害作用如氧化胁迫增加,降低抗氧化状态和线粒体氧化磷酸化功能障碍。这些数据表明,通过其有效的抗氧化剂和认知增强性能通过其通过喹啉酸引起的神经元障碍。

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