Schizophrenia is a chronic neuropsychiatric disorder with a poorly understood pathophysiology. The theories about the disorder are mainly about dysregulation in one or more systems of neurotransmitters, and the progression triggers the presence of inflammatory markers indicates the possibility that the disorder is initially an inflammatory disease. The objective was to evaluate the ascorbic acid supplementation in an animal model of schizophrenia, on behavioral parameters, and cytokines involved in inflammation IL-1β, IL-10. Wistar rats with 60 days of age were used which were supplemented with ascorbic acid at 0.1, 1, and 10 mg/kg or saline for 14 days via orogastric gavage. Subsequently, 4 groups were given ketamine (25mg/kg) and 4 groups received intraperitoneal saline from the 9th-15th day of the experiment. After 30 minutes of the last administration of ketamine/saline, and behavioral test, rats were killed by guillotine decapitation and the brain structures were carefully dissected for biochemical analysis. Results showed that ascorbic acid supplementation prevented motor sensory loss but nor alter other parameters evaluated. We concluded that ascorbic acid may be used as a therapeutic adjuvant in schizophrenia and may help to improve the schizophrenic patient's life quality.

中文翻译：

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补充抗坏血酸可减轻氯胺酮诱导的动物模型中的精神分裂症样症状

精神分裂症是一种慢性神经精神疾病，其病理生理学知之甚少。关于该疾病的理论主要是关于一个或多个神经递质系统的失调，进展引发炎症标志物的存在表明该疾病最初是一种炎症性疾病的可能性。目的是评估精神分裂症动物模型中抗坏血酸补充剂对行为参数和炎症 IL-1β、IL-10 中涉及的细胞因子的影响。使用 60 日龄的 Wistar 大鼠，通过口胃管饲法补充抗坏血酸 0.1、1 和 10 mg/kg 或生理盐水 14 天。随后，从实验的第9-15天开始，4组给予氯胺酮（25mg/kg），4组给予腹腔盐水。最后一次氯胺酮/生理盐水给药30分钟后，进行行为测试，断头断头处死大鼠，仔细解剖大脑结构进行生化分析。结果表明，补充抗坏血酸可防止运动感觉丧失，但也不会改变其他评估参数。我们得出结论，抗坏血酸可用作精神分裂症的治疗辅助剂，并可能有助于改善精神分裂症患者的生活质量。