Centella asiatica extract attenuates on glutamate-induced neurotoxicity in HT22 cells and scopolamine-induced animal model of cognitive impairment 9125

Abstract Description Centella asiatica, a traditional herb, is known for its neuroprotective, antioxidant, and anti-inflammatory properties. This study investigated the effects of Centella asiatica extract (CAE) on glutamate-induced neurotoxicity in HT22 cells and scopolamine-induced cognitive decline in mice. CAE protected hippocampal neuron-derived HT22 cells from glutamate-induced damage by reducing oxidative stress, regulating the expression of Bax and Bcl-2 proteins, and preventing neuronal apoptosis. Additionally, CAE increased the expression of brain-derived neurotrophic factor (BDNF) and cAMP response element-binding protein (CREB), a key transcription factor essential for neuronal differentiation. In vivo, oral administration of CAE significantly improved scopolamine-induced cognitive deficits in mice, as evidenced by Y-maze, novel object recognition, and passive avoidance tests. Biochemical analysis showed that CAE increased acetylcholine levels, decreased acetylcholinesterase activity in the hippocampus, enhanced antioxidant enzyme activity, and reduced malondialdehyde (MDA) levels in the cortex, highlighting its ability to enhance cholinergic function and mitigate oxidative stress. Furthermore, CAE upregulated BDNF expression in the CA3 region of the hippocampus. These results demonstrate that CAE alleviates cognitive dysfunction and exerts potent neuroprotective effects, suggesting its therapeutic potential for managing neurodegenerative diseases. Funding Sources This work was supported in part by grants from 3H LABS Corp. and the Korean Institute of Oriental Medicine (ERT2411220). Topic Categories Neuroimmunology (NEUR)