Nefazodone is an orally active phenylpiperazine antidepressant. Nefazodone can potently and selectively block postsynaptic 5-HT2A receptors, and moderately inhibit 5-HT and noradrenaline reuptake. Nefazodone can also relieve the adverse effects of stress on the the immune system of mice. Nefazodone has a high affinity for CYP3A4 isoenzyme, which indicates that it has certain risk of agent-agent interaction[1][2][3].
Nefazodone collapses mitochondrial membrane potential, and imposes oxidative stress, as detected via glutathione depletion, leading to cell death[2].
Nefazodone (200 μM; 24 h) depletes 100% of ATP in both, glucose and galactose-grown HepG2 cells[2].
Nefazodone (6.25, 12.5 and 25 μM; 0-120 min) profoundly inhibits oxygen consumption (OCR) in HepG2[2].
Nefazodone (10 mg/kg; s.c.; for 16 days) is effective to counter the adverse effects of stress on the the immune system of mice[3].
| Animal Model: | Female BALB/c mice (7-12 weeks old; stress model; subjected to a broad band noise at 100 dB daily for 5 s every minute during a 1- or 3-h period around midnight)[3] |
| Dosage: | 10 mg/kg |
| Administration: | s.c.; for 16 days |
| Result: | Attenuated the reduction of tmus, spleen and peripheral blood cellularity caused by stress. |
[1]. Davis R, et al. A review of its pharmacology and clinical efficacy in the management of major depression. Drugs. 1997 Apr;53(4):608-36.
[2]. Dykens JA, et al. In vitro assessment of mitochondrial dysfunction and cytotoxicity of nefazodone, trazodone, and buspirone. Toxicol Sci. 2008 Jun;103(2):335-45.
[3]. Freire-Garabal M, et al. Effects of nefazodone on the immune system of mice. Eur Neuropsychopharmacol. 2000 Jul;10(4):255-64.