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没食子酸对氯胺酮诱导精神分裂症模型的保护作用:可能的行为、生化、神经化学和细胞改变。

Protective effect of gallic acid in experimental model of ketamine-induced psychosis: possible behaviour, biochemical, neurochemical and cellular alterations.

机构信息

Department of Pharmaceutical Sciences, Faculty of Medical Sciences, Guru Jambheshwar University of Science and Technology, Hisar, 125001, India.

University Institute of Pharmaceutical Sciences, UGC Center of Advanced Study (UGC-CAS) in Pharmaceutical Sciences, Panjab University, Chandigarh, India.

出版信息

Inflammopharmacology. 2018 Apr;26(2):413-424. doi: 10.1007/s10787-017-0366-8. Epub 2017 Jun 2.

DOI:10.1007/s10787-017-0366-8
PMID:28577133
Abstract

Gallic acid has been reported to possess a number of psychopharmacological activities. These activities are attributed to the antioxidant potential due to the presence of phenolic moeity. The present study was carried out to investigate the protective effects of gallic acid in an experimental model of ketamine-induced psychosis in mice. Ketamine (50 mg/kg, i.p.) was used to induce stereotyped psychotic behavioural symptoms in mice. Behavioural studies (locomotor activity, stereotype behaviour, immobility duration and memory retention) were carried out to investigate the protective of gallic acid on ketamine-induced psychotic symptoms, followed by biochemical and neurochemical changes and cellular alterations in the brain. Chronic treatment with gallic acid for 15 consecutive days significantly attenuated stereotyped behavioural symptoms in mice. Biochemical estimations revealed that gallic acid reduced the lipid peroxidation and restored the total brain proteins. Furthermore, gallic acid remarkably reduced the dopamine levels, AChE activity and inflammatory surge (serum TNF-α), and increased the levels of GABA and increased glutathione in mice. The study revealed that gallic acid could ameliorate psychotic symptoms and biochemical changes in mice, indicating protective effects in psychosis.

摘要

没食子酸具有多种精神药理学活性。这些活性归因于由于酚部分的存在而具有的抗氧化潜力。本研究旨在研究没食子酸在氯胺酮诱导的小鼠精神病实验模型中的保护作用。氯胺酮(50mg/kg,ip)用于诱导小鼠刻板的精神病行为症状。进行行为研究(运动活动、刻板行为、不动时间和记忆保留),以研究没食子酸对氯胺酮诱导的精神病症状的保护作用,然后进行脑内生化和神经化学变化以及细胞改变。连续 15 天用没食子酸进行慢性治疗可显著减轻小鼠的刻板行为症状。生化评估显示,没食子酸可减少脂质过氧化并恢复总脑蛋白。此外,没食子酸可显著降低多巴胺水平、AChE 活性和炎症激增(血清 TNF-α),并增加 GABA 水平和增加小鼠的谷胱甘肽。该研究表明,没食子酸可改善小鼠的精神病症状和生化变化,表明其对精神病具有保护作用。

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