红藻氨酸
癫痫
抗惊厥药
丙戊酸
神经科学
化学
内分泌学
内科学
生物化学
生物
医学
谷氨酸受体
受体
作者
Qin Li,Yu‐Han Huang,Qiu-Qi Li,Ji-Ning Jia,Zhaoqian Liu,Honghao Zhou,Xinyu Zhou,Weilin Jin,Xiao‐Yuan Mao
出处
期刊:Neuroreport
[Ovid Technologies (Wolters Kluwer)]
日期:2024-10-01
标识
DOI:10.1097/wnr.0000000000002103
摘要
The objective of this study is to explore whether sodium valproate (VPA) alleviates epileptic seizures via suppressing lysyl oxidase (Lox)-mediated ferroptosis. Epileptic seizure mouse model was prepared via intrahippocampal injection of kainic acid (250 ng/μl). After treatment with kainic acid, VPA was injected intraperitoneally by the dose of 250 mg/kg twice daily for 4 days. Ferroptosis-associated indices including lipid peroxides (LPO) level and Ptgs2 mRNA in hippocampal tissue samples were detected. Additionally, effects of VPA on Lox mRNA and enzymatic activity were assessed by quantitative real-time PCR and a commercial kit, respectively. Neuronal survival was assessed by Nissl staining. In kainic acid-induced epileptic seizure mouse model, VPA significantly suppressed LPO level and Ptgs2 mRNA and the suppression of ferroptosis was positively correlated with its anti-seizure effect. Lox mRNA and enzymatic activity were also found to decrease in hippocampus of epileptic seizure mice after VPA treatment. Furthermore, overexpression of Lox via adeno-associated virus infection remarkably abrogated the inhibitory effect of VPA on ferroptosis and neuronal impairment together with its anti-seizure effect. VPA suppresses Lox-mediated ferroptosis process, which can provide the explanation for its anti-seizure property.
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