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抗坏血酸补充剂对氯胺酮诱导的精神分裂症动物模型中运动和乙酰胆碱酯酶活性的预防作用。

The preventive effects of ascorbic acid supplementation on locomotor and acetylcholinesterase activity in an animal model of schizophrenia induced by ketamine.

作者信息

Damazio Louyse S, Silveira Flávia R, Canever Lara, Castro Adalberto A DE, Estrela Jadne M, Budni Josiane, Zugno Alexandra I

机构信息

Programa de Pós-Graduação em Ciências da Saúde, Laboratório de Neurociências, Universidade do Extremo Sul Catarinense, Unidade Acadêmica de Ciências da Saúde, Av. Universitária, 1105, Bairro Universitário, 88806-000 Criciúma, SC, Brazil.

出版信息

An Acad Bras Cienc. 2017 Apr-Jun;89(2):1133-1141. doi: 10.1590/0001-3765201720160490. Epub 2017 May 15.

DOI:10.1590/0001-3765201720160490
PMID:28513779
Abstract

Studies have shown that schizophrenic patients seem to have nutritional deficiencies. Ascorbic acid (AA) has an important antioxidant effect and neuromodulatory properties. The aim of this study was to evaluate the effects of AA on locomotor activity and the acetylcholinesterase activity (AChE) in an animal model of schizophrenia (SZ). Rats were supplemented with AA (0.1, 1, or 10 mg/kg), or water for 14 days (gavage). Between the 9th and 15th days, the animals received Ketamine (Ket) (25 mg/kg) or saline (i.p). After the last administration (30 min) rats were subjected to the behavioral test. Brain structures were dissected for biochemical analysis. There was a significant increase in the locomotor activity in Ket treated. AA prevented the hyperlocomotion induced by ket. Ket also showed an increase of AChE activity within the prefrontal cortex and striatum prevented by AA. Our data indicates an effect for AA in preventing alterations induced by Ket in an animal model of SZ, suggesting that it may be an adjuvant approach for the development of new therapeutic strategies within this psychiatric disorder.

摘要

研究表明,精神分裂症患者似乎存在营养缺乏。抗坏血酸(AA)具有重要的抗氧化作用和神经调节特性。本研究的目的是评估AA对精神分裂症(SZ)动物模型中运动活动和乙酰胆碱酯酶活性(AChE)的影响。给大鼠补充AA(0.1、1或10mg/kg)或水,持续14天(灌胃)。在第9天至第15天期间,动物接受氯胺酮(Ket)(25mg/kg)或生理盐水(腹腔注射)。最后一次给药(30分钟)后,对大鼠进行行为测试。解剖脑结构进行生化分析。接受Ket治疗的大鼠运动活动显著增加。AA可预防Ket诱导的运动亢进。Ket还显示前额叶皮质和纹状体内AChE活性增加,而AA可预防这种增加。我们的数据表明,AA在预防SZ动物模型中Ket诱导的改变方面有作用,提示其可能是这种精神疾病新治疗策略开发的辅助方法。

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