Anti-Inflammatory Effects of Heliangin from Jerusalem Artichoke ( Helianthus tuberosus ) Leaves Might Prevent Atherosclerosis.
Papawee SaikiMizuki YoshiharaYasuhiro KawanoHitoshi MiyazakiKoyomi MiyazakiPublished in: Biomolecules (2022)
Atherosclerosis is considered the major cause of cardiovascular and cerebrovascular diseases, which are the leading causes of death worldwide. Excessive nitric oxide production and inflammation result in dysfunctional vascular endothelial cells, which are critically involved in the initiation and progression of atherosclerosis. The present study aimed to identify a bioactive compound from Jerusalem artichoke leaves with anti-inflammatory activity that might prevent atherosclerosis. We isolated bioactive heliangin that inhibited NO production in LPS-induced macrophage-like RAW 264.7 cells. Heliangin suppressed ICAM-1, VCAM-1, E-selectin, and MCP-1 expression, as well as NF-κB and IκBα phosphorylation, in vascular endothelial cells stimulated with TNF-α. These results suggested that heliangin suppresses inflammation by inhibiting excessive NO production in macrophages and the expression of the factors leading to the development of atherosclerosis via the NF-κB signaling pathway in vascular endothelial cells. Therefore, heliangin in Jerusalem artichoke leaves could function in the prevention of atherosclerosis that is associated with heart attacks and strokes.
Keyphrases
- signaling pathway
- lps induced
- endothelial cells
- cardiovascular disease
- induced apoptosis
- oxidative stress
- nitric oxide
- poor prognosis
- pi k akt
- inflammatory response
- type diabetes
- rheumatoid arthritis
- adipose tissue
- epithelial mesenchymal transition
- vascular endothelial growth factor
- atrial fibrillation
- cell proliferation
- nuclear factor
- physical activity
- cell death
- protein kinase
- hydrogen peroxide
- nitric oxide synthase