Evaluation of the antidepressant-like effect of musk in an animal model of depression: how it works.

Abstract

Depression has become a common public health problem that is showing increasing prevalence. Slow onset of action, low response rates and drug resistance are potential limitations of the current antidepressant drugs. Alternative therapy using natural substances, specifically aromatherapy, is currently tried to treat depression. This work aimed to assess the efficacy of musk in relieving the behavioral, biochemical and hippocampal histopathological changes induced by exposure to chronic mild stress in mice and explore the possible mechanism behind this antidepressant-like effect. Forty male albino mice were divided into four groups (n=10): control, a group exposed to chronic unpredictable mild stress (CUMS) and two groups exposed to CUMS and then treated with fluoxetine or musk. Behavioral changes and serum corticosterone levels were assessed at the end of the experiment. Protein and gene expressions of brain-derived neurotropic factor (BDNF) and glucocorticoid receptors (GRs) in the hippocampus were assessed using ELISA and real-time RT-PCR, respectively. Histopathological examination of the hippocampus and immunohistochemical techniques using glial fibrillary acidic protein (GFAP), Ki67, caspase-3, BDNF and GR were performed. Inhalation of musk had an antidepressant-like effect in an animal model of depression. Musk alleviated the behavioral changes and elevated serum corticosterone levels induced by exposure to chronic stress. It reduced the hippocampal neuronal apoptosis and stimulated neurogenesis in the dentate gyrus. Musk's action may be related to the upregulation of hippocampal GR and BDNF expressions. Musk is considered a potential antidepressant so it is advisable to assess its efficacy in treating depressed patient.