Homocysteine exaggerates microglia activation and neuroinflammation through microglia localized STAT3 overactivation following ischemic stroke

• Published in: Journal of neuroinflammation Vol. 14; no. 1; pp. 187 - 12
• Main Authors: Chen, Shuang, Dong, Zhiping, Cheng, Man, Zhao, Yaqian, Wang, Mengying, Sai, Na, Wang, Xuan, Liu, Huan, Huang, Guowei, Zhang, Xumei
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 18.09.2017; BioMed Central; BMC
• Subjects: Alzheimer's disease; Analysis; Animals; Brain; Brain injury; Brain Ischemia - metabolism; Brain Ischemia - pathology; Carotid arteries; Cell activation; Chlorides; Cytokines; Dentate gyrus; Development and progression; Gene expression; Genetic aspects; Homocysteine; Homocysteine - metabolism; Immunohistochemistry; Inflammation; Inflammation - metabolism; Inflammation - pathology; Interleukin 6; Ischemia; Ischemic brain; Janus kinase 2; Male; Microglia; Microglia - metabolism; Microglial cell; Microglial cells; Nervous system; Neural networks; Neurotoxicity; Phosphorylation; Physiological aspects; Rats; Rats, Sprague-Dawley; Reperfusion; Risk factors; Rodents; Signal transducers and activators of transcription 3; Signal transduction; Signal Transduction - physiology; Stat3 protein; STAT3 Transcription Factor - metabolism; Stroke; Stroke - metabolism; Stroke - pathology; Toxicity; Transcription; Triphenyltetrazolium chloride; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Veins & arteries; China; Microglial cell; Inflammation; Signal transducers and activators of transcription 3; Ischemic brain; Homocysteine

Elevated plasma homocysteine (Hcy) levels have been indicated as a strong and modifiable risk factor of ischemic stroke; the previous studies have shown that exposure to Hcy activates cultured microglia. However, whether neurotoxicity of Hcy involves microglia activation following brain ischemia and...