Abstract
Fenugreek (Trigonella Foenum-Graecum) seeds flavonoids (FSF) have diverse biological activities, while the antidepressant-like effect of FSF has been seldom explored. The aim of this study was to evaluate the antidepressant-like effect of FSF and to identify the potential molecular mechanisms. LC-MS/MS was used for the determination of FSF. Chronic restraint stress (CRS) was used to establish the animal model of depression. Observation of exploratory behavior in the forced swimming test (FST), tail suspension test (TST) and sucrose preference test (SPT) indicated the stress level. The serum corticosterone (CORT) level was measured. The monoamine neurotransmitters (5-HT, NE and DA) and their metabolites, as well as monoamine oxidase A (MAO-A) enzyme activity in the prefrontal cortex, hippocampus and striatum, were evaluated. The protein expression levels of KLF11, SIRT1, MAO-A were also determined by western blot analysis. The results showed that FSF treatment significantly reversed the CRS-induced behavioral abnormalities, including reduced sucrose preference and increased immobility time. FSF administration markedly restored CRS induced changes in concentrations of serum corticosterone, prefrontal cortex neurotransmitters (NE, 5-HT and DA), hippocampus neurotransmitters (NE, 5-HT and DA) and striatum neurotransmitters (NE). FSF treatment exhibited significant inhibition of MAO-A activity in the prefrontal cortex and hippocampus. FSF also significantly down-regulated the KLF11, SIRT1 and MAO-A protein expression levels in the prefrontal cortex and hippocampus. These findings indicate that FSF could exhibit an antidepressant-like effect by down-regulating the KLF11/SIRT1-MAO-A pathways, inhibiting MAO-A expression and activity, as well as up-regulating monoamine neurotransmitters levels.
Highlights
Depression, one of the most common mood disorders, has become one of the major causes of disability and will be the second most significant cause of disease by 2030 [1,2]
fenugreek seeds flavonoids (FSF) significantly down-regulated the KLF11, SIRT1 and monoamine oxidase A (MAO-A) protein expression levels in the prefrontal cortex and hippocampus. These findings indicate that FSF could exhibit an antidepressant-like effect by down-regulating the KLF11/SIRT1-MAO-A pathways, inhibiting
1, with increase of the concentration of ethanol extractsextracts from 7 plants, 7 plants, the inhibition rate of MAO-A gradually increased in the range of 0.25–32 mg/mL
Summary
Depression, one of the most common mood disorders, has become one of the major causes of disability and will be the second most significant cause of disease by 2030 [1,2]. Depression is characterized by mood disturbances, cognitive functions, anhedonia and attentional deficits [3]. An estimated 17–21% of the population has suffered from depression [4], and rapid social development will increase the risk factors that cause depression. The pathogenesis of depression is still intangible, some hypotheses have been put forward. The monoamine neurotransmitter hypothesis involves the core concepts of depression [5]. Studies have shown that lack of monoamine neurotransmitters, such as norepinephrine (NE), 5-hydroxytryptamine (5-HT), dopamine (DA), etc. Studies have shown that lack of monoamine neurotransmitters, such as norepinephrine (NE), 5-hydroxytryptamine (5-HT), dopamine (DA), etc. in the central and peripheral
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