Abstract
Rhodiola rosea L. (R. rosea) is an adaptogenic plant increasing body resistance to stress. Its efficacy has been evidenced mainly in chronic stress models, data concerning its effect in acute stress and underlying mechanisms being scarce. The objective was to investigate the effect of repeated doses of a R. rosea hydroethanolic root extract (HRE) on hypothalamic pituitary adrenal response in a murine model of acute mild stress and also the mechanisms involved. Stress response was measured in Balb/c mice having received by gavage HRE (5 g/kg) or vehicle daily for 2 weeks before being submitted to an acute mild stress protocol (open‐field test then elevated plus maze). Corticosterone was measured in plasma from mandibular vein blood drawn before and 30, 60, and 90 min after initiation of the stress protocol. Mice were sacrificed at 90 min, and the hippocampus, prefrontal cortex, and amygdala were excised for high‐frequency RT‐PCR gene expression analysis. At 30 min after acute mild stress induction, corticosterone level in mice having received the HRE was lower than in control mice and comparable to that in nonstressed mice in the HRE group. HRE administration induced brain structure‐dependent changes in expression of several stress‐responsive genes implicated in neuronal structure, HPA axis activation, and circadian rhythm. In the acute mild stress model used, R. rosea HRE decreased corticosterone level and increased expression of stress‐responsive genes, especially in the hippocampus and prefrontal cortex. These findings suggest that R. rosea HRE could be of value for modulating reactivity to acute mild stress.
Highlights
Stress is the physiological reaction to environmental threats or pressure and can be self‐driven or of external origin (Anghelescu, Edwards, Seifritz, & Kasper, 2018)
The objective of this study was to evaluate the effect on the HPA axis of chronic administration of a R. rosea hydroethanolic root extract (HRE) in a murine acute mild stress model by measuring corticosterone secretion and assessing cerebral expression of stress‐responsive genes
In the acute mild stress model used in this study, Balb/c mice were consecutively subjected to an OF and an elevated plus maze (EPM) test
Summary
Stress is the physiological reaction to environmental threats or pressure and can be self‐driven or of external origin (Anghelescu, Edwards, Seifritz, & Kasper, 2018). Modification of target gene transcription, the so‐called genomic action of corticosteroids, is most likely one of the main mechanisms underlying corticosteroid action in the brain (Gray, Kogan, Marrocco, & McEwen, 2017) These genomic effects can occur within 15–30 min after the activation of corticosteroid receptors and may last for less than an hour or up to several days, depending on the duration of exposure to the hormone and the type of stress (Dong, Poellinger, Gustafsson, & Okret, 1988; Morsink, Joels, et al, 2006). Characterizing the effects of R. rosea on the HPA axis and stress‐responsive gene transcription under acute mild stress conditions would contribute to a better understanding of how extracts of this adaptogenic plant act to prevent the negative effects of stress. The constituents of the R. rosea HRE were identified according to their retention times and mass spectral data and by comparison with authentic standards, if available, or otherwise with published data
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