Ginkgolide B ameliorates oxidized low-density lipoprotein-induced endothelial dysfunction via modulating Lectin-like ox-LDL-receptor-1 and NADPH oxidase 4 expression and inflammatory cascades
机构：[1]Department of Cardiovascular Medicine, Ninth Hospital of Xi'an, Xi'an, Shaanxi, 710054, China[2]Department of Cardiovascular Medicine, Shaanxi Second Provincal People's Hospital, Xi'an, Shaanxi, 710054, China[3]Department of cardiology, Xidian Group Hospital, Xi'an, Shaanxi, 710054, China[4]Department of Bioscience, Integral University, Lucknow, India[5]Medical Research and Laboratory Diagnostic Center, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong, 250013, China[6]Department of Vascular Surgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650032, China昆明医科大学附属第一医院
The current study was undertaken to delineate the protective effect of Ginkgolide B, a phyto-constituent from Ginkgo biloba, on oxidized (ox)-LDL-induced endothelial dysfunction via targeting Lectin-like ox-LDL-receptor-1 (LOX-1), NADPH oxidase 4 (NOX-4), and other inflammatory proteins. Our results have shown that Ginkgolide B downregulated the expression of LOX-1 in ox-LDL-treated human umbilical vein endothelial cells (HUVECs) and RAW246.7 murine macrophages which ultimately resulted in decreased cholesterol deposits in HUVECs and RAW264.7. Moreover, Ginkgolide B suppressed the enhanced NOX4 expression, which was associated with attenuation of ROS generation in ox-LDL-stimulated HUVECs and RAW264.7 cells. Ginkgolide B also ameliorated the endothelial dysfunction by inhibiting the augmented expression of monocyte chemotactic protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in ox-LDL-activated HUVECs. Furthermore, the enhanced expression of many inflammatory cytokines in ox-LDL-induced RAW264.7 macrophages, both at transcription and protein level, was significantly down-regulated after Ginkgolide B treatment. Ginkgolide B also illustrated atheroprotective property via suppressing the augmented expression of matrix metalloproteinase-1 and cyclooxygenase-2 in ox-LDL-stimulated RAW264.7 macrophages. In summary, our study has established that Ginkgolide B ameliorates endothelial dysfunction via targeting LOX-1, NOX-4, MCP-1, ICAM-1, and VCAM-1 along with the markers associated with inflammatory cascades and thus could be promoted as a valuable therapeutic agent in prevention and management of atherosclerosis.
第一作者机构：[1]Department of Cardiovascular Medicine, Ninth Hospital of Xi'an, Xi'an, Shaanxi, 710054, China
通讯作者：
通讯机构：[6]Department of Vascular Surgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650032, China[*1]Department of Vascular Surgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650032, China
推荐引用方式(GB/T 7714)：
Feng Zhanbin,Yang Xiaofei,Zhang Long,et al.Ginkgolide B ameliorates oxidized low-density lipoprotein-induced endothelial dysfunction via modulating Lectin-like ox-LDL-receptor-1 and NADPH oxidase 4 expression and inflammatory cascades[J].PHYTOTHERAPY RESEARCH.2018,32(12):2417-2427.doi:10.1002/ptr.6177.
APA：
Feng, Zhanbin,Yang, Xiaofei,Zhang, Long,Ansari, Irfan A.,Khan, M. Salman...&Feng, Yaoyu.(2018).Ginkgolide B ameliorates oxidized low-density lipoprotein-induced endothelial dysfunction via modulating Lectin-like ox-LDL-receptor-1 and NADPH oxidase 4 expression and inflammatory cascades.PHYTOTHERAPY RESEARCH,32,(12)
MLA：
Feng, Zhanbin,et al."Ginkgolide B ameliorates oxidized low-density lipoprotein-induced endothelial dysfunction via modulating Lectin-like ox-LDL-receptor-1 and NADPH oxidase 4 expression and inflammatory cascades".PHYTOTHERAPY RESEARCH 32..12(2018):2417-2427
