Abstract
Lindera obtusiloba extracts are commonly used as an alternative medicine due to its numerous health benefits in Korea. However, the antidepressant-like effects of L. obtusiloba extracts have not been fully elucidated. In this study, we aimed to determine whether L. obtusiloba extracts exhibited antidepressant-like activity in rats subjected to forced swim test (FST)-induced depression. Acute treatment of rats with L. obtusiloba extracts (200 mg/kg, p.o.) significantly reduced immobility time and increased swimming time without any significant change in climbing. Rats treated with L. obtusiloba extracts also exhibited a decrease in the limbic hypothalamic-pituitary-adrenal (HPA) axis response to the FST, as indicated by attenuation of the corticosterone response and decreased c-Fos immunoreactivity in the hippocampus CA3 region. In addition, L. obtusiloba extracts, at concentrations that were not affected by cell viability, significantly decreased luciferase activity in response to cortisol in a concentration-dependent manner by the glucocorticoid binding assay in HeLa cells. Our findings suggested that the antidepressant-like effects of L. obtusiloba extracts were likely mediated via the glucocorticoid receptor (GR). Further studies are needed to evaluate the potential of L. obtusiloba extracts as an alternative therapeutic approach for the treatment of depression.
Highlights
Continued and elevated glucocorticoid levels resulting from dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis is one of the most prominent neurobiological findings in depression [1,2]
We examined the antidepressant-like effects of L. obtusiloba extracts in forced swim test (FST)-induced depression in rats
Our results demonstrated that acute treatment with L. obtusiloba extracts significantly decreased the immobility time in rats exposed to the FST
Summary
Continued and elevated glucocorticoid levels resulting from dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis is one of the most prominent neurobiological findings in depression [1,2]. The glucocorticoid receptor (GR) mediates the direct effects of the glucocorticoids that are released in response to stress and regulates the HPA axis via a negative feedback mechanism in the hippocampus, hypothalamus, and pituitary gland [3,4]. Consistent with a role of glucocorticoids in depression, GR antagonists have been encouraged for potential therapeutic benefits in stress-related disorders. This is based on the ability of GR antagonists to block the increase in the levels of circulating glucocorticoids and on their ability to up-regulate GR [7]
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