Riparin II ameliorates corticosterone-induced depressive-like behavior in mice: Role of antioxidant and neurotrophic mechanisms
| Autor: | José Maria Barbosa Filho, Stanley Juan Chaves Gutierrez, Iris Cristina Maia Oliveira, Danielle Silveira Macêdo, Francisca Cléa Florenço de Sousa, Raquell de Castro Chaves, Daniel Moreira Alves da Silva, Mariana Albuquerque de Araujo, José Tiago Valentim, Alana Gomes de Souza, Iardja Stéfane Lopes, Victor Celso Cavalcanti Capibaribe |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
endocrine system
medicine.medical_specialty Elevated plus maze medicine.drug_class Tyramine Hippocampus Fluvoxamine Motor Activity medicine.disease_cause Anxiolytic Antioxidants Open field Mice 03 medical and health sciences Cellular and Molecular Neuroscience chemistry.chemical_compound 0302 clinical medicine Neurochemical Corticosterone Internal medicine medicine Animals Behavior Animal Depression business.industry Brain-Derived Neurotrophic Factor Cell Biology Antidepressive Agents 030227 psychiatry Disease Models Animal Oxidative Stress Endocrinology chemistry Benzamides Lipid Peroxidation business hormones hormone substitutes and hormone antagonists 030217 neurology & neurosurgery Oxidative stress medicine.drug |
| Zdroj: | Neurochemistry International. 120:33-42 |
| ISSN: | 0197-0186 |
| DOI: | 10.1016/j.neuint.2018.07.007 |
| Popis: | Riparin II (RIP II) is an alkamide isolated from Aniba riparia that has presented antidepressant and anxiolytic effects in acute stress behavioral models. This study aimed to investigate the activity of RIP II in a corticosterone-induced depression mice model. Corticosterone (20 mg/kg, s.c.) was administered once a day for 21 days. RIP II (50 mg/kg, p.o.) or fluvoxamine (FLU, 50 mg/kg, standard antidepressant, p.o.) was administered after corticosterone (CORT) injection, for the last 7 days of CORT treatment. Mice were exposed to the following behavioral tests: forced swimming, tail suspension, open field, sucrose preference, elevated plus maze and ymaze. After behavioral evaluation, brain areas (prefrontal cortex, hippocampus and striatum) were dissected for neurochemical evaluation: oxidative stress parameters (MDA, nitrite and GSH) and BDNF dosage. Repeated CORT administration caused depressive-like behavior in mice as indicated by increased despair effects in forced swimming and tail suspension tests and anhedonia in sucrose preference test. In addition, CORT decreased BDNF levels in the mice hippocampus and induced oxidative load in the brain with significative increase in pro-oxidant markers (lipid peroxidation and nitrite levels) and a decline in anti-oxidant defense system (reduced glutathione levels), indicating a direct effect of stress hormones in the induction of the brain oxidative stress. On the other hand, RIP II treatment reversed CORT-induced depressive-like behavior. Furthermore, this treatment reversed the impairment in BDNF levels and oxidative brain insults caused by CORT. This may demonstrate the mechanisms involved in antidepressant-like effect of RIP II. These findings further support that RIP II may be implicated as pharmacological intervention targeting depression associated with HPA-axis dysregulation. |
| Databáze: | OpenAIRE |
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