Excessive glutamate can cause oxidative stress in neuronal cells and this can significantly contribute to the etiology of neurodegenerative disease. The present study mainly aims to investigate that aloe extract (AE) and fermented aloe extract (FAE) could protect against glutamate-induced cytotoxicity by modulating oxidative stress. In this study, both AE and FAE showed potent neuroprotective activity by inhibiting ROS and Ca 2+ concentration, increasing mitochondria membrane potential, and activating glutathione-related enzymes against glutamate-insulted neurotoxicity in HT22 cells. In addition, the neuroprotective activity of FAE was more potent than that of AE. HPLC analysis reveals that the chemical composition of FAE is different from that of AE. Especially, the contents of aloin A, aloin B and aloenin were higher in FAE than in AE. In conclusion, this study indicates that both AE and FAE may have effective neuroprotective activity in glutamate-insulted pathological conditions such as Alzheimer’s disease by managing oxidative stress.

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Background Alzheimer’s disease (AD) is a type of dementia that leads to loss of memory and learning ability. Aloe arborescens is a traditional medicinal plant in Europe and Africa. It has been reported that A. arborescens showed anti-inflammatory, anti-cancer, antioxidant, and anti-obesity effects. Previously, we reported that fermented A. arborescens extract had neuroprotective activity in glutamate-insulted HT22 cells. Materials and Methods In this study, we evaluated its cognitive enhancing activity by using scopolamine-induced memory impairment in mice as a model system. Morris water maze test was carried out to evaluate spatial memory enhancing activity and a passive avoidance test was performed to evaluate an effect on learning memory. A. arborescens was extracted with methanol in an ultrasonic extraction device and fermented with Lactobacillus brevis. Fermented A. arborescens extract was treated to scopolamine-insulted Institute of Cancer Research (ICR) mice at a concentration of 100, 200, and 300 mg/kg, respectively. Results The fermented A. arborescens extract significantly improved the scopolamine-insulted memory impairment. Fermented A. arborescens extract inhibited acetylcholine esterase activity and boosted brain-derived neurotrophic factor and phosphorylated cAMP-response element-binding protein (p-CREB) expression. These results showed that fermented AA extract improved memory impairment through the increase of the BDNF and p-CREB signal pathway. Conclusion According to these results, we considered that the fermented A. arborescens extract can be a useful candidate for new nutraceuticals for improving memory impairment.