Antidepressant Potential of Masoi (Cryptocarya massoia) Essential Oil Aromatherapy

Abstract

Depression is a global mental health problem with a steadily increasing prevalence, while conventional therapies such as fluoxetine are often associated with side effects. Essential oil–based aromatherapy has been regarded as a promising natural alternative, including Cryptocarya massoia essential oil (MEO) originating from Papua. This oil contains massoialactone as its major bioactive compound, which is known to exhibit biological activities, including potential effects on the nervous system. However, scientific evidence regarding the antidepressant properties of MEO remains limited. This study aimed to evaluate the antidepressant potential of MEO inhalation in a corticosterone-induced mouse model. The effects were examined through a combination of behavioral, hormonal, and brain histopathological approaches. The working hypothesis was that MEO would reduce immobility time, suppress corticosterone levels, increase serotonin, and decrease apoptosis in the hippocampus and prefrontal cortex. Accordingly, this study was expected to provide preliminary evidence for the utilization of Indonesia’s natural resources in the development of antidepressant therapies. A total of 40 male DDY mice were divided into five groups consisted of normal, negative control, positive control (fluoxetine), test A (corticosterone + MEO), and test B (NaCl + MEO). Treatments were administered for 21 consecutive days, with MEO inhalation at 5% concentration for one hour per day. Evaluations were carried out using the Tail Suspension Test and Forced Swim Test, measurement of corticosterone and serotonin levels by ELISA, and brain histopathological analysis with H&E staining. The chemical composition of MEO was determined using gas chromatography–mass spectrometry (GC–MS). The results indicated that massoialactone was the dominant component of MEO. Inhalation of MEO did not produce statistically significant differences in immobility time, corticosterone, or serotonin levels compared with the negative control. However, biological trends were observed toward reduced immobility and corticosterone and increased serotonin. Histopathological analysis revealed no significant changes in apoptosis within the hippocampus or prefrontal cortex, but the number of cells in the olfactory bulb of the MEO groups was significantly lower than that of the normal and positive control groups. This finding suggests potential local cytotoxic effects on olfactory tissue caused by MEO exposure. In conclusion, this study provides preliminary evidence that MEO contains active components with the potential to influence biological pathways related to depression, although the effects were not statistically significant. The important novel finding of olfactory bulb involvement highlights the need for careful consideration of safety aspects. Therefore, further studies with larger sample sizes, dose variations, and comprehensive toxicological evaluations are required before MEO can be developed as a candidate for antidepressant aromatherapy.