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摘要:
Percutaneous coronary intervention is a well-established technique used to treat coronary artery disease,but the risk of coronary artery in-stent restenosis following percutaneous coronary intervention is still high.Previous studies revealed that high mobility group protein B1(HMGB1)plays a critical role in neointima formation.In this study,we aimed to investigate the role of glycyrrhizic acid(GA),an HMGB1 inhibitor,in the process of neointima formation and the potential mechanisms.We investigated the role of GA in neointima formation through an iliac artery balloon injury model in rabbits.Proliferation,migration,and phenotype transformation of human vascular smooth muscle cells(VSMCs)were observed.Besides,infl ammation and receptor for advanced glycosylation end products(RAGE)signaling pathways were studied.The results indicate that GA attenuated neointima formation and downregulated HMGB1 expression in injured artery in rabbits.HMGB1 promoted proliferation,migration,and phenotype transformation through the activation of RAGE signaling pathways in VSMCs,and blockade of HMGB1 by GA(1,10,and 100μM)could attenuate those processes and reduce proliferation of human VSMCs.In conclusion,the HMGB1 inhibitor GA might be useful to treat proliferative vascular diseases by downregulating RAGE signaling pathways.Our results indicate a new and promising therapeutic agent for restenosis.
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篇名 Glycyrrhizic Acid Attenuates Balloon-Induced Vascular Injury Through Inactivation of RAGE Signaling Pathways
来源期刊 Cardiovascular Innovations and Applications 学科 医学
关键词 Glycyrrhizic acid high mobility group protein B1 infl ammation vascular smooth muscle cell receptor for advanced glycosylation end products
年,卷(期) 2020,(2) 所属期刊栏目
研究方向 页码范围 239-249
页数 11页 分类号 R54
字数 语种
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节点文献
Glycyrrhizic
acid
high
mobility
group
protein
B1
infl
ammation
vascular
smooth
muscle
cell
receptor
for
advanced
glycosylation
end
products
研究起点
研究来源
研究分支
研究去脉
引文网络交叉学科
相关学者/机构
期刊影响力
Cardiovascular Innovations and Applications
季刊
2009-8618
Beijing Anzhen Hospi
出版文献量(篇)
42
总下载数(次)
0
总被引数(次)
0
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