病态的
冲程(发动机)
氧化磷酸化
缺血性中风
大鼠模型
自噬
医学
炎症
氧化应激
大脑中动脉
大脑皮层
免疫组织化学
病理
神经炎症
谷胱甘肽
脑缺血
神经保护
基因表达
免疫系统
脑梗塞
皮质(解剖学)
中枢神经系统
内分泌学
老化
闭塞
缺血性损伤
信使核糖核酸
脑梗塞
小胶质细胞
神经科学
促炎细胞因子
麻醉
缺血
内科学
脑动脉
作者
Ola A. Habotta,Ahmed Abdeen,Basma M. Hendam,Heba M. Elhessy,Lamiaa M. Elabbasy,Basma Othman,Ruba Almaghrabi,Hind A. Alzahrani,Samah F. Ibrahim,Helal F. Hetta,Rasha E. Azab,Noor A Mohmand,Kasim Sakran Abass,Majed Aldehri,Hind Zafrah,Mohamed Abomosallam
标识
DOI:10.1038/s41598-025-08178-w
摘要
Ischemic stroke is globally acknowledged as a prominent reason for disability and mortalities. Oxidative stress, neuroinflammation, and autophagy have been implicated in its pathogenesis. A model of middle cerebral artery occlusion (MCAO) in male rats was conducted for this investigation and the brain cortex was sampled taken after at 1, 6, 12, 24, and 48 h of IRI. The results revealed time-dependent decreases in cortical GSH with rises in MDA and NO levels. Additionally, marked upregulations of inflammatory cytokines were observed and increased as time progressed. Besides, significant upregulations in TLR4, GFAP, Iba-1, and BDNF mRNA expressions were noticed along with increases in the P62 and decreases in LC3 immune expression levels. The pathological findings of cerebral sections showed vacuolations in the neuropil, perivascular edema, and shrinkage of neurons which also increased gradually by time. Taken together, these biomarkers could be reliable indicators for determination of time elapsed after IRI.
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