Baicalin Ameliorates L‐Glutamate‐Induced Hippocampal Oxidative Stress Injury and Apoptosis in Mice by Regulating Nrf2/HO‐1 Signalling Pathway

This study aimed to explore the effect and mechanism of baicalin on L-glutamate-induced oxidative stress injury in the hippocampus of mice. Forty mice were divided into five groups:Sham, model, N-acetyl-L-cysteine (NAC) and baicalin (BA-7.5 mg/kg and BA-15 mg/kg). A model of excitatory amino acid toxicity with oxidative stress injury was induced by injecting L-glutamate into the lateral ventricle. Drugs were administered intraperitoneally post-modelling. Six hours later, behavioural tests were performed. Brain lesions were observed via HE staining, and neuronal apoptosis was evaluated using TUNEL staining. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were determined using biochemical methods. Fluorescent staining was employed to detect the expression of reactive oxygen species (ROS). The expression of Cytochrome C (CytC) was assessed by immunohistochemistry. The levels of Nrf2, HO-1, SOD2 and catalase (Cat) were detected by qPCR and WB. The behavioural tests showed that the motion distance and pain threshold were reduced in the model group. MDA, ROS and CytC were increased, while SOD and Cat were decreased after modelling. The CA3 region of the hippocampus exhibited pathological changes, and the rate of TUNEL-positive increased. Baicalin could reverse these changes, especially BA-7.5 mg/kg. Baicalin can reduce the injury induced by L-glutamate, and the mechanism might be related to the activation of the Nrf2/HO-1 pathway.