愤怒(情绪)
医学
神经炎症
小胶质细胞
神经保护
糖基化
受体
冲程(发动机)
促炎细胞因子
星形胶质细胞
缺血
免疫学
β淀粉样蛋白
血脑屏障
内科学
脑梗塞
发病机制
作者
Bin Liu,Guoliang Liu,Wang Yueyang,Yuan Yao,Guanzhuo Wang,Xia Lei,Ning Zhang,Dong Xiaohong
出处
期刊:Medical Science Monitor
[International Scientific Information, Inc.]
日期:2019-10-18
卷期号:25: 7813-7825
被引量:4
摘要
BACKGROUND The aim of this study was to investigate the protective mechanism of neurovascular unit of Buyang Huanwu decoction (BYHWD) in an Alzheimer's disease (AD) cell model via RAGE/LRP1 pathway and find a reliable target for Alzheimer's disease treatment. MATERIAL AND METHODS Rat brain microvessel endothelial cells (BMECs) were cultured in 10% FBS and 1% penicillin/streptomycin. The AD model was established by administration of 24 μmol/L amyloid-s peptides 25~35. Different concentrations of BYHWD (0.1 mg/mL, 1 mg/mL, and 10 mg/mL) were added as the drug intervention. The morphology of the cells was observed by light microscopy and the ultrastructure of the cells was observed by microscopy. The inflammatory factors IL-1s, IL-6, TNF-alpha, and As25-35 were detected by ELISA. Flow cytometry was used to assess the apoptosis rate. The expressions of RAGE, LRP1, ICAM-1, VCAM-1, Apo J, Apo E, and NF-kappaBp65 were detected by Western blotting. RESULTS The structure of cells in BYHWDM and BYHWDH gradually recovered with increasing dose. BYHWD decreased the apoptotic rate of BMECs induced by As25-35. The cells treated with different concentrations of BYHWD had significant difference in terms of anti-apoptotic effect. The therapeutic effect of BYHWD on AD was via the RAGE/LRP1 and NF-kappaBp65 pathways. CONCLUSIONS BYHWD regulates As metabolism via the RAGE/LRP1 pathway, inhibits vascular endothelial inflammation induced by ICAM-1 and VCAM-1 via the NF-kappaBP65 pathway, and promotes morphological changes induced by As-induced brain microvascular endothelial cell damage.
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