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

// Kun-Ling Tsai 1,* , Ching-Hsia Hung 1,2,* , Shih-Hung Chan 3 , Jhih-Yuan Shih 4 , Yung-Hsin Cheng 5 , Yi-Ju Tsai 1 , Huei-Chen Lin 2,6 and Pei-Ming Chu 7 1 Department of Physical Therapy, College of Medicine, National Cheng Kung University, Tainan, Taiwan 2 Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan 3 Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan 4 Department of Internal Medicine, Chi-Mei Hospital, Tainan, Taiwan 5 Department of Education and Research, Taipei City Hospital, Taipei, Taiwan 6 Department of Physical Therapy, Shu-Zen Junior College Of Medicine And Management, Taiwan 7 Department of Anatomy, School of Medicine, China Medical University, Taichung, Taiwan * These authors have contributions equally to this work Correspondence to: Pei-Ming Chu, email: // Keywords : atherosclerosis, ROS, endothelial cells, lectin-like oxidized LDL receptor 1, baicalein, Gerotarget Received : July 06, 2016 Accepted : October 13, 2016 Published : October 20, 2016 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.