Abstract
Purpose: To investigate the antidepressant mechanism of action of Crassifoside H (CH) from the rhizomes of Curculigo glabrescens (Hypoxidaceae) in chronic unpredictable mild stress (CUMS)-induced rats.Methods: CUMS-induced rat depressant model was established. Behavioral tests, viz, sucrose preference test (SPT), open field test (OFT) and forced swimming test (FST) were applied to assess the antidepressant effect of CH. Enzyme linked immunosorbent assay (ELISA) was used to assess thelevels of corticosterone (CORT), TNF-α and IL-1β in serum. Protein expressions of TNF-α, IL-1β and NLRP3 in rat hippocampus were determined by Western blot.Results: Crassifoside H significantly ameliorated CUMS-induced depressant-like behavior as the serum CORT level of CUMS rats. CH remarkably decreased TNF-α and IL-1β levels in serum and hippocampus of CUMS rats. Moreover, Crassifoside H significantly inhibited NLRP3 activation inhippocampus.Conclusion: The findings demonstrate that Crassifoside H has antidepressant effect on CUMS rats. The mechanism of action of CH may be at least partly due to the improvement of hypothalamic-pituitaryadrenal (HPA) axis dysfunction by decreasing serum CORT. These findings suggest that Crassifoside H has a therapeutic potential for the management of depression.
 Keywords: Crassifoside H, Antidepression, Curculigo glabrescens, Hypoxidaceae, Hypothalamicpituitary- adrenal axis, Inflammation, Corticosterone
Highlights
Depression is a common psychiatric disease with high prevalence and heavily influences patient’s health and life, and imposes huge burden on individuals, families and society [1]
Crassifoside H (CH) administration improved depressant-like behavior of chronic unpredictable mild stress (CUMS)-treated rats In forced swimming test (FST), rats were separately put in a glass vessel (60 cm tall, 25 cm diameter) filled with water with depth of 30 cm to swim 5 min
Characteristic depressive-like behavior was observed in the experiments including sucrose preference test (SPT), open field test (OFT) and FST; while CH administration significantly alleviated the behavioral abnormality in CUMS rats
Summary
Depression is a common psychiatric disease with high prevalence and heavily influences patient’s health and life, and imposes huge burden on individuals, families and society [1]. Increasing evidence suggests that depression is a neuroinflammatory disorder, and several inflammation-related cytokines are implicated in the development of this disease [3]. The inflammatory cytokines, i.e. interleukin-1 beta (IL1β), tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6), are high level in depressed patients [4]. Inflammatory cytokines are involved in the dysfunction of hypothalamicpituitary-adrenal (HPA) axis, cerebral noradrenergic systems and brain serotonergic systems in depressed patients [5]. IL-1β is the first reported inflammatory cytokine that cause the hyper-activation of HPA axis in depression [6]. TNF-α is another important inflammatory cytokine involved in depression by influencing activity of HPA axis and serotonin metabolism. Some antidepressants displayed the ability to restore the disorders of HPA axis and TNF-α [7]
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