Baicalein protects against oxLDL-caused oxidative stress and inflammation by modulation of AMPK-alpha.

Kun-Ling Tsai,Yung-Hsin Cheng,Ching-Hsia Hung,Shih-Hung Chan,Jhih-Yuan Shih,Yi-Ju Tsai,Pei-Ming Chu,Huei-Chen Lin

doi:10.18632/oncotarget.12788

Abstract

Atherosclerosis is considered to be a form of chronic inflammation and a disorder of lipid metabolism. Oxidative transformations in the lipid and apolipoprotein B (Apo B) constituent of low density lipoprotein drive the initial step in atherogenesis due to macrophage scavenger receptors identify oxidized LDL (oxLDL) but non-oxidized LDL. The human vascular endothelial cells fact a critical role in vasodilation, provides a nonadhesive surface for circulation, reduces vascular smooth muscle proliferation, inflammation, thrombus formation and platelet aggregation. Assembly of oxLDL contribute to stimulation of endothelial cells with up-regulation of adhesion molecules, increase oxidative stress to the vascular endothelium and inhibition of NO-mediated vasodilation. When adhesion molecules are over-expressed on the surface of endothelial cells under oxLDL stimulation, it will recruit monocytes to the arterial wall. Then adherent monocytes will migrate into the subendothelial space and subsequently differentiate into macrophages. In the subendothelial space, oxLDL will be taken up by macrophages, thereby causing the substantial cholesterol accumulation and the foam cells production.

Highlights

Atherosclerosis is considered to be a form of chronic inflammation and a disorder of lipid metabolism [1]
We aimed to explore whether Baicalein could mitigate LOX-1-drived human endothelial dysfunction by the up-regulation of NADPH oxidase, and if so, whether AMPK was involved in the process
Treatment of Human umbilical vein endothelial cells (HUVECs) with baicalein for 2 hrs at concentrations above 2.5 μM before exposure to oxidized LDL (oxLDL) for 24 hrs resulted in suppression of LOX-1 expression both in protein levels (Figure 1)

Summary

Introduction

Atherosclerosis is considered to be a form of chronic inflammation and a disorder of lipid metabolism [1]. The human vascular endothelial cells act a critical role in vasodilation, provides a nonadhesive surface for circulation, reduces vascular smooth muscle proliferation, inflammation, thrombus formation and platelet aggregation [3]. Of oxLDL contribute to stimulation of endothelial cells with up-regulation of adhesion molecules, increase oxidative stress to the vascular endothelium and inhibition of NOmediated vasodilation [4]. When adhesion molecules are over-expressed on the surface of endothelial cells under oxLDL stimulation, it will recruit monocytes to the arterial wall. Adherent monocytes will migrate into the subendothelial space and subsequently differentiate into macrophages [5]. OxLDL will be taken up by macrophages, thereby causing the substantial cholesterol accumulation and the foam cells production [6]

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Conclusion