Selvaraj Baskar Kim, Dae Won Yoo, Ki-Yeon Park, Keunwan Thi Thu Thuy Tran Lee, Jae Wook Lee, Heesu 2024-04-25T08:10:04Z 2024-04-25T08:10:04Z 2024-04-25 2024-03 1226-7155 https://pubs.kist.re.kr/handle/201004/149749 Glutamate-mediated oxidative stress causes neuronal cell death by increasing intracellular Ca 2+ uptake, reactive oxidative species (ROS) generation, mitogen-activated protein kinase (MAPK) activation, and translocation of apoptosis-inducing factor (AIF) to the nucleus. In the current study, we demonstrated that corydaline exerts potent neuroprotective effects against glutamate-induced neurotoxicity. Treatment with 5 mmol/L glutamate increased cellular Ca 2+ influx, ROS generation, MAPK activation, and AIF translocation. In contrast, corydaline treatment decreased cellular Ca 2+ influx and ROS generation. Western blot analysis revealed that glutamate-mediated MAPK activation was attenuated by corydaline treatment. We further demonstrated that corydaline treatment inhibited the glutamate-mediated translocation of AIF to the nucleus. We propose that corydaline is a promising lead structure for the development of safe and effective neuroprotectants. English 대한구강생물학회 Neuroprotective Mechanism of Corydaline in Glutamate-Induced Neurotoxicity in HT22 Cells Article 10.11620/IJOB.2024.49.1.10 2 International Journal of Oral Biology, v.49, no.1, pp.10 - 17 International Journal of Oral Biology 49 1 10 17 N kci other ART003064313 HT22 mouse hippocampal neuronal cells Corydaline Glutamate-induced neurotoxicity