Protective effects of camellia oil and gac oil against corticosterone-induced neurotoxicity in Neuro-2a cells

Abstract

Depression is characterized by the hyperaccumulation of glucocorticoids, such as corticosterone (CORT), which results in oxidative stress, inflammatory responses, and nerve damage. Edible camellia oil (Camellia oleifera Abel.) and gac oil (Momordica cochinchinensis Spreng) contain beneficial bioactive compounds, such as oleic acid, polyphenols, flavonoids, tocopherol, β-carotene, and lycopene, which have neuroprotective effects. However, the underlying mechanisms of camellia oil (CO) and gac oil (GO) in alleviating CORT-induced depressive-like effects are still unclear. Therefore, this study aimed to investigate the effects of CO and GO on CORT-induced damage in Neuro-2a cells. The results revealed that the upregulation of proapoptotic-associated proteins (Bax, cleaved caspase 9, cleaved caspase 3, cytochrome c), cyclooxygenase-2, interleukin-1β, reactive oxygen species, and malondialdehyde levels in CORT-stimulated Neuro-2a cells was significantly counteracted by CO and GO treatment, which enhanced the production of antiapoptotic Bcl-2, the antioxidative enzymes superoxide dismutase, catalase, glutathione peroxidase, glutathione, heat shock proteins (HSP32, HSP 60, HSP 90), and glucocorticoid receptor (GR)/brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB)/extracellular signal-regulated kinase (ERK)/cAMP response element-binding protein (CREB). These findings suggest that increasing daily CO and GO consumption may suppress CORT-induced depression.