Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.24.3 (
collagenase
)
18,340
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
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.
...
PMID: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. 3013 46