Suppr超能文献

丁香酸通过激活 p38 丝裂原活化蛋白激酶缓解丙戊酸诱导的自闭症:可能的分子途径。

Syringic acid alleviates valproic acid induced autism via activation of p38 mitogen-activated protein kinase: Possible molecular approach.

机构信息

Neuropharmacology division, Department of Pharmacology, ISF College of Pharmacy, Moga, India.

出版信息

Environ Toxicol. 2023 Oct;38(10):2400-2415. doi: 10.1002/tox.23876. Epub 2023 Jun 26.

Abstract

Autism spectrum disorder (ASD) is a multifactorial neurodevelopmental disorder characterized by restrictive and repetitive behavior followed by impairment in social, verbal, and non-verbal interaction and communication. Valproic acid (VPA) is a well-known anti-epileptic drug, but its prenatal exposure to animals causes social impairment, neurotransmitters imbalance, and neuroinflammation with ASD-like phenotypes. Syringic acid (SA) is a polyphenolic compound with anti-inflammatory, anti-apoptotic, antioxidant, and neuromodulator activity. The purpose of study was to investigate the protective effect of Syringic acid (SA) in prenatal VPA-treated rats through behavioral, neuroinflammation, oxidative stress, neurotransmitters, neuronal integrity, and apoptotic marker. Single dose of VPA was administered 600 mg/kg, i.p. on a gestational day (GD) 12th and SA was administrated from PnD 26th to 54th at the dose of 25, 50, and 100 mg/kg, p.o. On PnD 56th behavioral parameters (Pain sensitivity, open field test, narrow beam walks test and social impairment test) were performed and all animals were sacrificed, and brain tissue was isolated for oxidative stress (GSH, CAT, and LPO), neuroinflammation (TNF-α and IL-6) and neurotransmitters (GABA and Glutamate), histopathology (H&E, Nissl), immunohistochemistry (p38 MAPK) analysis. Rat treated with SA dose-dependently prevented behavioral alteration, restored antioxidant enzymes, neurotransmitters level, decreased neuroinflammatory markers, and improved neuronal integrity. Furthermore, immunohistochemistry confirmed the reduced p38 MAPK marker expression by SA in VPA induced autistic behavior.

摘要

自闭症谱系障碍 (ASD) 是一种多因素神经发育障碍,其特征是限制和重复行为,随后是社会、言语和非言语交流和沟通障碍。丙戊酸 (VPA) 是一种众所周知的抗癫痫药物,但动物在产前接触 VPA 会导致社交障碍、神经递质失衡、神经炎症和 ASD 样表型。丁香酸 (SA) 是一种多酚化合物,具有抗炎、抗凋亡、抗氧化和神经调节作用。本研究旨在通过行为、神经炎症、氧化应激、神经递质、神经元完整性和凋亡标志物研究丁香酸 (SA) 对产前 VPA 处理大鼠的保护作用。单次给予 VPA 600mg/kg,ip,于妊娠第 12 天(GD),SA 于 PnD 26 至 54 天给予,剂量为 25、50 和 100mg/kg,po。于 PnD 56 进行行为参数(疼痛敏感性、旷场试验、狭窄梁行走试验和社交障碍试验),并对所有动物进行安乐死,分离脑组织进行氧化应激(GSH、CAT 和 LPO)、神经炎症(TNF-α 和 IL-6)和神经递质(GABA 和谷氨酸)、组织病理学(H&E、Nissl)、免疫组织化学(p38 MAPK)分析。SA 以剂量依赖的方式治疗大鼠可预防行为改变,恢复抗氧化酶、神经递质水平,降低神经炎症标志物,并改善神经元完整性。此外,免疫组织化学证实 SA 可减少 VPA 诱导的自闭症行为中的 p38 MAPK 标志物表达。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验