Abstract
BackgroundMusk (Moschus moschiferus) has been described to have a significant impact on the central nervous system, as well as anticonvulsion and antidepressant effects. This study was designed to evaluate the efficacy of musk in alleviating alterations induced in olfactory bulb of depressed mice exposed to chronic stress and identify the mechanism behind it.MethodsFifty male albino mice were divided into five groups (n = 10 each): control, musk, chronic unpredictable mild stress (CUMS), fluoxetine-treated, and musk-treated groups were included in this study. Behavioral changes and serum levels of corticosterone and proinflammatory cytokines included tumor necrosis factor α, interleukin 6, and oxidant/antioxidant profile were assessed at the end of the experiment. Main olfactory bulb (MOB) has been processed for histopathological examination. Gene expression of caspase-3, glial fibrillary acidic protein, and Ki67 were assessed in the MOB using quantitative real-time polymerase chain reaction.ResultsThe study showed that musk inhalation significantly reduced (p < 0.001) corticosterone level, immobility time, inflammatory cytokines, and oxidative stress markers in CUMS-exposed mice compared to the untreated CUMS group. Musk lessened CUMS-associated neuronal alterations in the MOB and significantly reduced apoptosis and enhanced neural cell proliferation (p < 0.001) comparable to fluoxetine. Musk significantly enhanced the level of antioxidants in the serum and significantly reduced inflammatory cytokines. The anti-inflammatory and antioxidant activity of musk and its constituents seemed to be behind its neuroprotective effect observed in this study.ConclusionMusk effectively ameliorated the chronic stress–induced behavioral, biochemical, and neuronal structural changes in MOB mostly through its antioxidant and anti-inflammatory effect.
Highlights
Depression is considered a worldwide health problem as more than 264 million from different age groups, all over the world, are suffering from depression
The study showed that musk inhalation significantly reduced (p < 0.001) corticosterone level, immobility time, inflammatory cytokines, and oxidative stress markers in chronic unpredictable mild stress (CUMS)-exposed mice compared to the untreated CUMS group
Musk and Olfactory Bulb in Depressed Mice activity of musk and its constituents seemed to be behind its neuroprotective effect observed in this study
Summary
Depression is considered a worldwide health problem as more than 264 million from different age groups, all over the world, are suffering from depression. Olfactory perceptual deficits are reported in several neurodegenerative disorders as Alzheimer disease, vascular dementia, Parkinson disease, and frontotemporal dementia These deficits appear early and preceding the classical cognitive and motor symptoms of the disease; they are considered as prodromal symptoms. These deficits are accompanied by pathology in related brain regions, for example, the limbic system, amygdala, hippocampus, and neocortical areas (Rey et al, 2018; Yoo et al, 2018). Exposure to chronic stress has been described to impair neurogenesis in hippocampus of rodents and subsequently involved in pathogenesis of neurodegenerative disorders as major depression that has been improved by use of antidepressants (Boldrini et al, 2009; Ayuob et al, 2018). This study was designed to evaluate the efficacy of musk in alleviating alterations induced in olfactory bulb of depressed mice exposed to chronic stress and identify the mechanism behind it
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