Neuroprotective effects of vetiver oil against corticosterone-induced cell death in human neuroblastoma SH-SY5Y cells through antioxidant activity
Keywords:
Depression, Vetiver oil, Caspase-3, Lactate dehydrogenase, Cell viability, AntioxidantsAbstract
Abstract
Vetiver oil is known to reduce stress and depression. The pathophysiology of depression is associated with neuronal damage, especially from increased free radicals. Therefore, the aim of this study was to investigate the antioxidant activities of vetiver oil on corticosterone-induced apoptosis in neuroblastoma SH-SY5Y cells. The cells were treated with 650 μM of corticosterone in the absence or the presence of vetiver oil (0.025, 0.05, 0.1, 0.25, 0.5, 1, 1.5, 2.5, 5 μg/ml) compared with fluoxetine 10 μM for 24 hours. Cell viability was measured by MTT assay. Lactate dehydrogenase (LDH), caspase-3 and reactive oxygen species (ROS) were investigated by spectrometry and ELISA techniques, respectively. Corticosterone significantly decreased cell viability while vetiver oil (0.1 μg/ml) significantly reversed the decreased viability induced by corticosterone. Cells treated with corticosterone significantly increased LDH release, but vetiver oil at 0.025, 0.05, 0.5, 0.1, 0.25 and 0.5 μg/ml and fluoxetine 10 μM attenuated increased LDH
release from cells due to corticosterone-induced cytotoxicity. Interestingly, corticosterone significantly increased caspase-3, while vetiver oil but not fluoxetine attenuated this increase. Vetiver oil (0.025, 0.05, 0.5, 0.1, 0.25, 0.5 μg/ml) and fluoxetine suppressed intracellular ROS was induced by corticosterone. The findings demonstrated that vetiver oil had a neuroprotective effect. The mechanism by which the neuroprotective effects of vetiver on corticosterone-induced neurotoxicity in SH-SY5Y cells may involve antioxidant activity.
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