biostudies-literatureUnknown13(1)Hu SOxidative stress is considered as an important mechanism underlying the pathology of neurodegenerative disorders. In this study, we utilized an <i>in vitro</i> model where oxidative stress process was evoked by exogenous hydrogen peroxide (H₂O₂) in HT22 murine hippocampal neurons and evaluated the neuroprotective effects of geissoschizine methyl ether (GME), a naturally occurring alkaloid from the hooks of <i>Uncaria rhynchophylla</i> (Miq.) Jacks. After a 24 h H₂O₂ (350 μM) insult, a significant decrease in cell survival and a sharp increase in intracellular reactive oxygen species were observed in HT22 cells. Encouragingly, GME (10-200 μM) effectively reversed these abnormal cellular changes induced by H₂O₂. Moreover, mechTranslational neuroscience369-378https://www.ebi.ac.uk/biostudies/studies/S-EPMC9552775biostudies-literatureProtection against H₂O₂-evoked toxicity in HT22 hippocampal neuronal cells by geissoschizine methyl ether via inhibiting ERK pathway.PMC9552775Wen XWu ZHu SLi ZYang LMa YLi LfalseProtection against H₂O₂-evoked toxicity in HT22 hippocampal neuronal cells by geissoschizine methyl ether via inhibiting ERK pathway.Oxidative stress is considered as an important mechanism underlying the pathology of neurodegenerative disorders. In this study, we utilized an <i>in vitro</i> model where oxidative stress process was evoked by exogenous hydrogen peroxide (H₂O₂) in HT22 murine hippocampal neurons and evaluated the neuroprotective effects of geissoschizine methyl ether (GME), a naturally occurring alkaloid from the hooks of <i>Uncaria rhynchophylla</i> (Miq.) Jacks. After a 24 h H₂O₂ (350 μM) insult, a significant decrease in cell survival and a sharp increase in intracellular reactive oxygen species were observed in HT22 cells. Encouragingly, GME (10-200 μM) effectively reversed these abnormal cellular changes induced by H₂O₂. Moreover, mech2022-01-01T00:00:00Z2022 Jan2025-06-01T01:16:39.084Z2024-11-13T21:57:11.971ZS-EPMC95527753630409810.1515/tnsci-2022-0243