Effect of "rose essential oil" inhalation on stress-induced skin-barrier disruption in rats and humans.

In stressed animals, several brain regions (e.g., hypothalamic paraventricular nucleus [PVN]) exhibit neuronal activation, which increases plasma adrenocorticotropic hormone (ACTH) and glucocorticoids. We previously reported that so-called "green odor" inhibits stress-induced activation of the hypothalamo-pituitary-adrenocortical axis (HPA axis) and thereby prevents the chronic stress-induced disruption of the skin barrier. Here, we investigated whether rose essential oil, another sedative odorant, inhibits the stress-induced 1) increases in PVN neuronal activity in rats and plasma glucocorticoids (corticosterone [CORT] in rats and cortisol in humans) and 2) skin-barrier disruption in rats and humans. The results showed that in rats subjected to acute restraint stress, rose essential oil inhalation significantly inhibited the increase in plasma CORT and reduced the increases in the number of c-Fos-positive cells in PVN. Inhalation of rose essential oil significantly inhibited the following effects of chronic stress: 1) the elevation of transepidermal water loss (TEWL), an index of the disruption of skin-barrier function, in both rats and humans and 2) the increase in the salivary concentration of cortisol in humans. These results suggest that in rats and humans, chronic stress-induced disruption of the skin barrier can be limited or prevented by rose essential oil inhalation, possibly through its inhibitory effect on the HPA axis.

Green odor and depressive-like state in rats: toward an evidence-based alternative medicine?

It is widely accepted that mental stress is an important factor in the development of psychological disorders such as depression. On pre-existing evidence, the so-called green odor may have a relieving and sedative effect on animals exposed to stressful situations. Using two behavioral models of depression, the forced-swim test and learned helplessness paradigm, we investigated whether inhalation of green odor (a 50:50 mixture of trans-2-hexenal and cis-3-hexenol) might alleviate and/or prevent experimentally induced depressive-like states in rats. A 3-min swim every day for 7 days resulted in significant prolongation of immobility time (vs. day 1). Inhaling green odor, but not vehicle, thereafter for 10 days (without swimming) led to the prolonged immobility time being significantly reduced and the hippocampal level of brain-derived neurotrophic factor (BDNF) being significantly increased. In the learned helplessness paradigm, the failure number and time spent in the shock compartment seen in the active avoidance test were both significantly attenuated in those rats that inhaled green odor for 11 days after the postshock screening test (vs. vehicle-exposed rats). Finally, for 10 consecutive days rats continuously exposed to green odor or vehicle swam for 3 min/day. Immobility time was significantly shorter in the green-odor group than in the vehicle-exposed group on days 6-10. These results suggest that green odor has not only a therapeutic, but also a preventive effect on depressive-like states in rats. These effects may be at least in part due to a green odor-induced upregulation of BDNF in the hippocampus.

Effects of central injection of angiotensin-converting-enzyme inhibitor and angiotensin type 1 receptor antagonist on the brain NF-kappaB and AP-1 activities of rats given LPS.

Angiotensin II (ANG II) activation of the angiotensin type 1 (AT1) receptor facilitates the production of brain interleukin-1beta (IL-1beta) and contributes to the induction of the fever following the intracerebroventricular (i.c.v.) injection of lipopolysaccharide (LPS). The purpose of the present study was to investigate whether proinflammatory transcription factors [nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1)] contribute to the ANG II-dependent production of cytokines within the brain. Interestingly, we found that a single i.c.v. injection of LPS had no effect on NF-kappaB and AP-1 activities in the hypothalamus, hippocampus, and cerebellum at either 1 or 3 h post-injection (except for a decrease in hypothalamic AP-1 activity at 1 h). Furthermore, both an angiotensin-converting-enzyme (ACE) inhibitor and an AT1 receptor antagonist enhanced (rather than reduced) the NF-kappaB and AP-1 activities in the hippocampus and/or cerebellum of rats given LPS. In contrast, an i.c.v. injection of ANG II increased the NF-kappaB activity in the hypothalamus. These results suggest that while "endogenous" ANG II exerts (via AT1 receptors) inhibitory effects on the activation of transcription factors in the brain of rats given LPS, a large dose of exogenous ANG II produces effects opposite to those induced by the presumably small amount of endogenous ANG II released locally by LPS. Our results seem not to support the idea that NF-kappaB and AP-1 play key roles in the ANG II-induced enhancement of the production of proinflammatory cytokines that is induced by LPS in the rat's brain.