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Neuroprotective effects of Shaoyao Gancao decoction against excitatory damage in PC12 cells based on the Src-NR2-nNOS pathway

作     者:Xiaoxu Fan Hongyan Ma Tiantian Zhou Min Fu Zhiyuan Qiao Yingtong Feng Zhen Wang Yiwei Shen Jingxia Wang 

作者机构:School of Traditional Chinese MedicineBeijing University of Chinese MedicineBeijing 102488China School of Traditional Chinese MedicineXinjiang Medical UniversityUrumqi 830017China The Centre for Translational BiologyResearch Institute of McGill University Health CentreMontréal H4A 3J1Canada 

出 版 物:《Journal of Traditional Chinese Medical Sciences》 (中医科学杂志(英文))

年 卷 期:2024年第11卷第3期

页      面:293-302页

学科分类:1008[医学-中药学(可授医学、理学学位)] 1006[医学-中西医结合] 100602[医学-中西医结合临床] 10[医学] 

基  金:supported by the National Natural Science Foundation of China(82074036) 

主  题:Shaoyao Gancao decoction PC12 N-Methyl-D-aspartic acid(NMDA) γ-aminobutyric acid(GABA) Src nNOs 

摘      要:Objective:To explore the neuroprotective effects of the Shaoyao Gancao decoction(SGD)against excitatory damage in PC12 cells and the role of the Src-NR2-nNOS pathway mediation by SGD in regulatingγ-aminobutyric acid(GABA)-glutamate(Glu)***: N-Methyl-d-aspartic acid(NMDA)was used to establish a PC12 cell excitability injury *** investigate the neuroprotective effect of SGD,a cell counting kit-8(CCK-8)assay was used to determine PC12 cell viability,Annexin V/Propidium Iodide(Annexin V/PI)double staining was used to determine PC12 cell apoptosis,and Ca^(2+)concentration was observed using laser confocal *** receptor agonists and antagonists were used to analyze the neuroprotective interactions betweenγ-aminobutyric acid(GABA)and NMDA ***,molecular biology techniques were used to determine mRNA and protein expression in the Src-NR2-nNOS *** analyzed the correlations between the regulatory sites of GABA and NMDA interactions,excitatory neurotoxicity,and brain damage at the molecular ***: NMDA excitotoxic injury manifested as a significant decrease in cell activity,increased apoptosis and caspase-3 protein expression,and a significant increase in intracellular Ca^(2+)*** of SGD,a GABAA receptor agonist(muscimol),or a GABAB receptor agonist(baclofen)decreased intracellular Ca^(2+)concentrations,attenuated apoptosis,and reversed NMDA-induced upregulation of caspase-3,Src,NMDAR2A,NMDAR2B,and ***,a GABA_(A)receptor antagonist(bicuculline)and a GABA_(B)receptor antagonist(saclofen)failed to significantly increase excitatory ***: Taken together,these results not only provide an experimental basis for SGD administration in the clinical treatment of central nervous system injury diseases,but also suggest that the Src-NR2A-nNOS pathway may be a valuable target in excitotoxicity treatment.

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