Neuroprotective and Antioxidant Effects of Riparin I in a Model of Depression Induced by Corticosterone in Female Mice
| Autor: | Gabriel Carvalho Rodrigues, Natália Ferreira de Oliveira, José Maria Barbosa-Filho, Auriana Serra Vasconcelos Mallmann, Francisco Adelvane de Paula Rodrigues, Raquell de Castro Chaves, Marta Maria de França Fonteles, Victor Celso Cavalcanti Capibaribe, Iris Cristina Maia Oliveira, Stanley Juan Chavez Gutierrez, Laura Maria Teodorio Vidal, Iardja Stéfane Lopes Sales, Alyne Mara Rodrigues de Carvalho, Francisca Cléa Florenço de Sousa |
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| Rok vydání: | 2020 |
| Předmět: |
endocrine system
Context (language use) Pharmacology medicine.disease_cause Neuroprotection Hippocampus Antioxidants chemistry.chemical_compound Mice Neurochemical Corticosterone medicine Animals Biological Psychiatry Brain-derived neurotrophic factor Behavior Animal business.industry Depression Brain-Derived Neurotrophic Factor Psychiatry and Mental health Disease Models Animal Neuropsychology and Physiological Psychology Mood chemistry Antidepressant Female business Oxidative stress |
| Zdroj: | Neuropsychobiology. 81(1) |
| ISSN: | 1423-0224 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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