Neuroprotective and Antioxidant Effects of Riparin I in a Model of Depression Induced by Corticosterone in Female Mice.

IF 2.3 4区心理学 Q3 NEUROSCIENCES Neuropsychobiology Pub Date : 2022-01-01 Epub Date: 2021-04-29 DOI:10.1159/000515929

Iris Cristina Maia Oliveira, Auriana Serra Vasconcelos Mallmann, Francisco Adelvane de Paula Rodrigues, Laura Maria Teodorio Vidal, Iardja Stéfane Lopes Sales, Gabriel Carvalho Rodrigues, Natalia Ferreira de Oliveira, Raquell de Castro Chaves, Victor Celso Cavalcanti Capibaribe, Alyne Mara Rodrigues de Carvalho, Marta Maria de França Fonteles, Stanley Juan Chavez Gutierrez, José Maria Barbosa-Filho, Francisca Cléa Florenço de Sousa

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引用次数: 6

Abstract

Background: Depression is a common, chronic, and often recurrent serious mood disorder. Conventional antidepressants present limitations that stimulate the search for new drugs. Antioxidant and neuroprotective substances are potential antidepressant agents. In this context, riparin I (RIP I) has presented promising results, emerging as a potential source of a new therapeutic drug. In this study, the antidepressant effect of RIP I was evaluated in an animal model of depression induced by corticosterone (CORT). The involvement of neuroprotective and antioxidant mechanisms in the generation of this effect was also assessed.

Methods: Female mice were submitted to CORT for 21 days and treated with RIP I in the last 7 days. Behavioral and neurochemical analyses were performed.

Results: The administration of RIP I reversed the depressive and psychotic-like behavior, as well as the cognitive impairment caused by CORT, in addition to regulating oxidative stress parameters and BDNF levels in depression-related brain areas.

Conclusion: These findings suggest that RIP I can be a strong candidate for drugs in the treatment of depression.

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利帕林1在皮质酮诱导的雌性小鼠抑郁模型中的神经保护和抗氧化作用。

背景:抑郁症是一种常见的、慢性的、经常复发的严重情绪障碍。传统的抗抑郁药存在局限性，这刺激了对新药的研究。抗氧化剂和神经保护物质是潜在的抗抑郁药物。在这种背景下，利帕林I (RIP I)已经呈现出令人鼓舞的结果，成为一种新的治疗药物的潜在来源。本研究在皮质酮(CORT)诱导的抑郁动物模型中评估RIP I的抗抑郁作用。还评估了神经保护和抗氧化机制在产生这种效应中的作用。方法:雌性小鼠给予CORT 21 d，最后7 d给予RIP 1。进行行为和神经化学分析。结果:RIP I的使用逆转了抑郁和精神样行为，以及CORT引起的认知障碍，此外还调节了抑郁相关脑区的氧化应激参数和BDNF水平。结论:这些发现提示RIP I可能是治疗抑郁症的有力候选药物。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neuropsychobiology 医学-精神病学

CiteScore

7.20

自引率

0.00%

发文量

审稿时长

6 months

期刊介绍： The biological approach to mental disorders continues to yield innovative findings of clinical importance, particularly if methodologies are combined. This journal collects high quality empirical studies from various experimental and clinical approaches in the fields of Biological Psychiatry, Biological Psychology and Neuropsychology. It features original, clinical and basic research in the fields of neurophysiology and functional imaging, neuropharmacology and neurochemistry, neuroendocrinology and neuroimmunology, genetics and their relationships with normal psychology and psychopathology. In addition, the reader will find studies on animal models of mental disorders and therapeutic interventions, and pharmacoelectroencephalographic studies. Regular reviews report new methodologic approaches, and selected case reports provide hints for future research. ''Neuropsychobiology'' is a complete record of strategies and methodologies employed to study the biological basis of mental functions including their interactions with psychological and social factors.