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• W2086768977 endingPage "57" @default.
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• W2086768977 abstract "Taking into account that pro-inflammatory cytokines and oxidative and nitrosative stress are implicated in the pathogenesis of depression and that α-tocopherol has antidepressant, anti-inflammatory and antioxidant properties, this study investigated the ability of α-tocopherol to abolish the depressive-like behavior induced by i.c.v. administration of TNF-α in the mouse TST. Additionally, we investigated the occurrence of changes in the levels of Bcl2 and Bax and phosphorylation of GSK-3β (Ser9) in the hippocampus of mice. The administration of TNF-α (0.001 fg/site, i.c.v.) increased the immobility time in the TST, which was prevented by the administration of α-tocopherol at the doses of 10, 30 and 100 mg/kg (p.o.). Subeffective doses of α-tocopherol (10 mg/kg, p.o.) and/or the antidepressants fluoxetine (5 mg/kg, p.o.), imipramine (0.1 mg/kg, p.o.) and bupropion (1 mg/kg, p.o.), the NMDA receptor antagonist MK-801 (0.001 mg/kg, p.o.) or the neuronal nitric oxide synthase inhibitor 7-nitroindazole (25 mg/kg, i.p.) prevented the depressive-like effect induced by TNF-α. None of the treatments altered the locomotor activity of mice. Treatment with TNF-α and/or α-tocopherol did not alter the levels of Bax and Bcl2 or the phosphorylation of GSK-3β in the hippocampus of mice. Together, our results show a synergistic antidepressant-like effect of α-tocopherol with antidepressants against the depressive-like behavior induced by an inflammatory insult, suggesting that this vitamin may be useful to optimize conventional pharmacotherapy of depression, including depressive states associated with inflammatory conditions." @default.
• W2086768977 created "2016-06-24" @default.
• W2086768977 creator A5000302901 @default.
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• W2086768977 date "2013-10-01" @default.
• W2086768977 modified "2023-10-17" @default.
• W2086768977 title "Antidepressant-like effect of α-tocopherol in a mouse model of depressive-like behavior induced by TNF-α" @default.
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