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

IF 2.7 4区医学 Q2 PHARMACOLOGY & PHARMACY

Basic & Clinical Pharmacology & Toxicology Pub Date : 2025-03-20 DOI:10.1111/bcpt.70024

Feng Li, Zishan Huang, Huanyu Gou, Jiarui Zheng, Mingjiang Yao

{"title":"Baicalin Ameliorates L-Glutamate-Induced Hippocampal Oxidative Stress Injury and Apoptosis in Mice by Regulating Nrf2/HO-1 Signalling Pathway","authors":"Feng Li, Zishan Huang, Huanyu Gou, Jiarui Zheng, Mingjiang Yao","doi":"10.1111/bcpt.70024","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Objective</h3>\n \n <p>This study aimed to explore the effect and mechanism of baicalin on L-glutamate-induced oxidative stress injury in the hippocampus of mice.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>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.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>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.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>Baicalin can reduce the injury induced by L-glutamate, and the mechanism might be related to the activation of the Nrf2/HO-1 pathway.</p>\n </section>\n </div>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"136 4","pages":""},"PeriodicalIF":2.7000,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Basic & Clinical Pharmacology & Toxicology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/bcpt.70024","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}

引用次数: 0

Abstract

Objective

This study aimed to explore the effect and mechanism of baicalin on L-glutamate-induced oxidative stress injury in the hippocampus of mice.

Methods

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.

Results

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.

Conclusion

Baicalin can reduce the injury induced by L-glutamate, and the mechanism might be related to the activation of the Nrf2/HO-1 pathway.

查看原文本刊更多论文

黄芩苷通过调节Nrf2/HO-1信号通路改善L-谷氨酸诱导的小鼠海马氧化应激损伤和细胞凋亡

研究目的本研究旨在探讨黄芩苷对L-谷氨酸诱导的小鼠海马氧化应激损伤的影响及机制：方法：将40只小鼠分为5组：Sham组、模型组、N-乙酰-L-半胱氨酸组（NAC）和黄芩苷组（BA-7.5 mg/kg和BA-15 mg/kg）。向侧脑室注射 L-谷氨酸，诱导兴奋性氨基酸毒性氧化应激损伤模型。建模后腹腔注射药物。六小时后进行行为测试。通过 HE 染色观察脑损伤，并使用 TUNEL 染色评估神经元凋亡。使用生化方法测定超氧化物歧化酶（SOD）和丙二醛（MDA）的水平。荧光染色法用于检测活性氧（ROS）的表达。细胞色素 C（CytC）的表达采用免疫组化法进行评估。通过 qPCR 和 WB 检测 Nrf2、HO-1、SOD2 和过氧化氢酶（Cat）的水平：结果：行为测试表明，模型组的运动距离和疼痛阈值降低。建模后，MDA、ROS和CytC增加，SOD和Cat减少。海马CA3区出现病理变化，TUNEL阳性率增加。黄芩苷能逆转这些变化，尤其是 BA-7.5 mg/kg：结论：黄芩苷能减轻L-谷氨酸诱导的损伤，其机制可能与激活Nrf2/HO-1通路有关。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Basic & Clinical Pharmacology & Toxicology 医学-毒理学

CiteScore

5.60

自引率

6.50%

发文量

126

审稿时长

1 months

期刊介绍： Basic & Clinical Pharmacology and Toxicology is an independent journal, publishing original scientific research in all fields of toxicology, basic and clinical pharmacology. This includes experimental animal pharmacology and toxicology and molecular (-genetic), biochemical and cellular pharmacology and toxicology. It also includes all aspects of clinical pharmacology: pharmacokinetics, pharmacodynamics, therapeutic drug monitoring, drug/drug interactions, pharmacogenetics/-genomics, pharmacoepidemiology, pharmacovigilance, pharmacoeconomics, randomized controlled clinical trials and rational pharmacotherapy. For all compounds used in the studies, the chemical constitution and composition should be known, also for natural compounds.