Baicalin ameliorated glutamate toxicity-induced nerve damage in mouse-derived hippocampal neuronal HT22 cells

Abstract

Baicalin, a flavonoid isolated from Scutellaria baicalensis, has anti-inflammatory, antioxidant, and neuroprotective effects. Glutamate is a major neurotransmitter that plays an important role in brain function, but excessive release of glutamate causes excitotoxicity and damages cells. We investigated the neuroprotective effects of baicalin in glutamate-exposed neurons. The mouse hippocampal neuronal cell line (HT22) was cultured in a general manner, glutamate and/or baicalin were treated on the cells. Baicalin was administered 1 hr before glutamate treatment. Cells were collected 24 hr after glutamate, and cell viability was measured using MTT assay. Reactive oxygen species (ROS) and lipid peroxidation (LPO) assays were performed to measure oxidative stress. Glutamate reduced cell viability in a dose- and time-dependent manner. MTT assay showed that baicalin treatment ameliorated the decrease in cell viability due to glutamate toxicity. The effect of baicalin is dose-dependent. Glutamate caused severe nerve damage, including condensation of the cell shape, loss of dendrites and axons. However, baicalin treatment attenuated these morphological changes, and the effect of baicalin was dose-dependent. ROS and LPO analyses showed that glutamate increases oxidative stress, and baicalin attenuates this change due to glutamate toxicity. The effect of baicalin on these results was dose-dependent. We confirmed that baicalin performs an antioxidant function against glutamate toxicity in neurons. In conclusion, these results suggest that baicalin exerts neuroprotective effects on damaged neurons through antioxidant activity.