Open AccessGlycyrrhizic Acid Attenuates Balloon-Induced Vascular Injury Through Inactivation of RAGE Signaling Pathways
Author(s) -
Zhaowei Zhu,
Yanan Guo,
Xuping Li,
Shuai Teng,
Xiaofan Peng,
Pu Zou,
Shenghua Zhou
Publication year - 2020
Publication title -
cardiovascular innovations and applications
Language(s) - English
Resource type - Journals
eISSN - 2009-8782
pISSN - 2009-8618
DOI - 10.15212/cvia.2019.0577
Subject(s) - neointima , hmgb1 , restenosis , rage (emotion) , vascular smooth muscle , medicine , signal transduction , inflammation , percutaneous coronary intervention , microbiology and biotechnology , pharmacology , cancer research , immunology , stent , biology , neuroscience , myocardial infarction , smooth muscle
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, inflammation 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 100 μM) 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.