Anti-Inflammatory Effects of Heliangin from Jerusalem Artichoke (Helianthus tuberosus) Leaves Might Prevent Atherosclerosis.

Papawee Saiki,Hitoshi Miyazaki,Mizuki Yoshihara,Yasuhiro Kawano,Koyomi Miyazaki

doi:10.3390/biom12010091

Abstract

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.

Highlights

Cardiovascular diseases (CVDs) are the most prevalent cause of death, accounting for ~31% of all deaths worldwide [1]
The results showed that heliangin suppressed the levels of p-nuclear factor κ-light-chain-enhancer of activated B cell (NF-κB) and p-IκBα induced by TNF-α, but could not suppress p38 mitogen-activated protein kinase (MAPK) and JNK1/2 (Figure 4)
The MAPK and NF-κB signaling pathways are involved in regulating the function of endothelial cells and might be key factors in the formation of arteriosclerosis [48,49], our results suggested that heliangin could suppress TNF-α effects in vascular endothelial cells via the NF-κB signaling pathway

Summary

Introduction

Cardiovascular diseases (CVDs) are the most prevalent cause of death, accounting for ~31% of all deaths worldwide [1] Such diseases include ischemic heart disease, heart failure, peripheral arterial disease, stroke, and atherosclerosis, which are major contributors to a reduced quality of life [2,3,4]. Thereafter, monocytes differentiate into macrophages and are transformed into foam cells These foam cells secrete proinflammatory cytokines and eventually undergo apoptosis. This process leads to inflammation and progressive atheroma formation [5,6]. Foam cell apoptosis is an important feature of atherosclerotic plaque development [6] This series of events indicates that anti-inflammatory activity in macrophages is important to prevent atherosclerosis. We evaluated the inhibition of NO production in RAW

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