Cinara Ludvig Gonçalves1, Helena Mendes Abelaira2, Thayse Rosa2, Airam Barbosa de Moura2, Deise Cristina Veron2, Laura Araújo Borba2, Maria Eduarda Mendes Botelho2, Mariana Pereira Goldim3, Leandro Garbossa3, Maria Eduarda Fileti3, Fabricia Petronilho3, Zuleide Maria Ignácio2,4,5, João Quevedo2,6,7,8, Gislaine Zilli Réus9. 1. Experimental Neurology Laboratory, Graduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, SC, Brazil. 2. Translational Psychiatry Laboratory, Graduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, SC, 88806-000, Brazil. 3. Neurobiology of Metabolic and Inflammatory Processes Laboratory, Graduate Program in Health Sciences, University of South Santa Catarina, Tubarão, SC, Brazil. 4. Laboratory of Physiology, Pharmacology and Psychopathology, Campus Chapecó, Federal University of South Frontier (UFFS), Chapecó, Santa Catarina, Brazil. 5. State Secretary for Justice and Citizenship of Santa Catarina, Chapecó, Brazil. 6. Department of Psychiatry and Behavioral Sciences, Center of Excellence On Mood Disorders, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, USA. 7. Translational Psychiatry Program, Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, USA. 8. Neuroscience Graduate Program, Graduate School of Biomedical Sciences, The University of Texas Health Science Center At Houston (UTHealth), Houston, TX, USA. 9. Translational Psychiatry Laboratory, Graduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, SC, 88806-000, Brazil. gislainereus@unesc.net.
Abstract
BACKGROUND: Electroconvulsive therapy (ECT) is often recommended for major depressive disorder (MDD) for those who do not respond to the first and second antidepressant trials. A combination of two therapies could improve antidepressant efficacy. Thus, this study aimed to investigate the synergistic effects of ECT combined to antidepressants with a different mechanism of action. METHODS: Rats were treated once a day, for five days with ketamine (5 mg/kg), fluoxetine (1 mg/kg), and bupropion (4 mg/kg) alone or in combination with ECT (1 mA; 100 V). After, oxidative damage and antioxidant capacity were assessed in the prefrontal cortex (PFC) and hippocampus, and pro-inflammatory cytokines levels were evaluated in the serum. RESULTS: ECT alone increased lipid peroxidation in the PFC and hippocampus. In the PFC of rats treated with ECT in combination with fluoxetine and bupropion, and in the hippocampus of rats treated with ECT combined with ketamine and bupropion there was a reduction in the lipid peroxidation. The nitrite/nitrate was increased by ECT alone but reverted by combination with ketamine in the hippocampus. Superoxide dismutase (SOD) was increased by ECT and maintained by fluoxetine and bupropion in the PFC. ECT alone increased interleukin-1β (IL-1β) and the administration of ketamine was able to revert this increase showing a neuroprotective effect of this drug when in combination with ECT. CONCLUSION: The treatment with ECT leads to an increase in oxidative damage and alters the immunological system. The combination with ketamine was able to protect against oxidative damage and the immunological response induced by ECT.
BACKGROUND: Electroconvulsive therapy (ECT) is often recommended for major depressive disorder (MDD) for those who do not respond to the first and second antidepressant trials. A combination of two therapies could improve antidepressant efficacy. Thus, this study aimed to investigate the synergistic effects of ECT combined to antidepressants with a different mechanism of action. METHODS:Rats were treated once a day, for five days with ketamine (5 mg/kg), fluoxetine (1 mg/kg), and bupropion (4 mg/kg) alone or in combination with ECT (1 mA; 100 V). After, oxidative damage and antioxidant capacity were assessed in the prefrontal cortex (PFC) and hippocampus, and pro-inflammatory cytokines levels were evaluated in the serum. RESULTS: ECT alone increased lipid peroxidation in the PFC and hippocampus. In the PFC of rats treated with ECT in combination with fluoxetine and bupropion, and in the hippocampus of rats treated with ECT combined with ketamine and bupropion there was a reduction in the lipid peroxidation. The nitrite/nitrate was increased by ECT alone but reverted by combination with ketamine in the hippocampus. Superoxide dismutase (SOD) was increased by ECT and maintained by fluoxetine and bupropion in the PFC. ECT alone increased interleukin-1β (IL-1β) and the administration of ketamine was able to revert this increase showing a neuroprotective effect of this drug when in combination with ECT. CONCLUSION: The treatment with ECT leads to an increase in oxidative damage and alters the immunological system. The combination with ketamine was able to protect against oxidative damage and the immunological response induced by ECT.
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