Potent protection of Danshensu（β-3,4-dihydroxyphenyl-lactic acid）against excitotoxic effects of maternal intragastric administration of monosodium glutamate at a late stage of pregnancy on developing mouse fetal brain

• Published in: Neural regeneration research Vol. 5; no. 20; pp. 1559 - 1567
• Main Author: Jingen Shen Lijian Yu Rundi Ma Yongping Zhang Xiaoyu Zhang Juanzhi Fang Tingxi Yu
• Format: Journal Article
• Language: English
• Published: 2010
• Subjects: 丹参素; 二羟基苯; 保护作用; 兴奋作用; 大脑发育; 怀孕后期
• ISSN: 1673-5374

Recent studies have demonstrated that ferulic acid[3-（4-hydroxy-3-methoxyphenyl）-2-propenoic acid]and sodium ferulate produce protective effects against glutamate-induced neurotoxicity in adult mice.Danshensu（β-3,4-dihydroxyphenyl-lactic acid）has a similar molecular structure and pharmacological action to caffeic acid.This study aimed to validate the protection conferred by Danshensu against excitotoxic effects of maternal intragastric administration of monosodium glutamate at late stages of pregnancy in the developing mouse fetal brain.Behavioral tests,as well as histopathological and immunohistochemical examination of hippocampi were performed in filial mice.Results revealed that maternal intragastric administration of excessive monosodium glutamate（1.0,2.0,4.0 g/kg body weight）at a late stage of pregnancy resulted in a series of behavioral disorders（hyperactivity,lesions of learning and memory,and disturbance in cooperation of movement ability under high-altitude stress）,histopathological impairment（neuronal edema,degeneration,necrosis,and hyperplasia）and molecular cellular biological changes（upregulated expression of N-methyI-D-aspartate receptor type 1 and neuropeptide Y in the hippocampal region of the brain of the filial mice from mothers treated with monosodium glutamate）.Simultaneous administration of sodium Danshensu partially reversed the effects of monosodium glutamate on the above mentioned phenomena.These findings indicate that sodium Danshensu exhibits obvious protective effects on the excitotoxicity of monosodium glutamate.