Suppressive Effects of the Gynura bicolor Ether Extract on Endothelial Permeability and Leukocyte Transmigration in Human Endothelial Cells Induced by TNF- α

Shu-Ling Hsieh; Jyh-Jye Wang; Kuan-Hua Su; Ying-Lan Kuo; Shuchen Hsieh; Chih-Chung Wu

doi:10.1155/2020/9413724

Suppressive Effects of the Gynura bicolor Ether Extract on Endothelial Permeability and Leukocyte Transmigration in Human Endothelial Cells Induced by TNF- α

Evid Based Complement Alternat Med. 2020 Dec 22:2020:9413724. doi: 10.1155/2020/9413724. eCollection 2020.

Authors

Shu-Ling Hsieh¹, Jyh-Jye Wang², Kuan-Hua Su³, Ying-Lan Kuo¹, Shuchen Hsieh⁴, Chih-Chung Wu⁵

Affiliations

¹ Department of Seafood Science, National Kaohsiung University of Science and Technology, Kaohsiung 81157, Taiwan.
² Department of Nutrition and Health Science, Fooyin University, Kaohsiung 83102, Taiwan.
³ Graduate Institute of Medical Sciences, Chang Jung Christian University, Tainan 71101, Taiwan.
⁴ Department of Chemistry, National Sun Yat-Sen University, Kaohsiung 80424, Taiwan.
⁵ Department of Food and Nutrition, Providence University, Taichung 43301, Taiwan.

Abstract

Gynura bicolor (Roxb. and Willd.) DC (G. bicolor) is generally used as a dietary vegetable and traditional herb in Taiwan and the Far East. G. bicolor exerts antioxidant and anti-inflammatory effects and regulates blood lipids and cholesterol. However, the effects of G. bicolor on endothelial transmigration and atherosclerosis are not clear. The present study investigated the effects of G. bicolor on endothelial permeability and transmigration in human endothelial cells. We prepared G. bicolor ether extract (GBEE) for use as the experimental material. Under TNF-α stimulation, HL-60 cell adherence to EA.hy926 cells, the shape of EA.hy926 cells, and the expression of adhesion molecules and transmigration-related regulatory molecules were analysed after pretreatment with GBEE for 24 h. GBEE inhibited leukocyte adhesion to endothelial cells, reduced intercellular adhesion molecule-1 (ICAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1) expressions, and decreased endothelial monolayer permeability. GBEE also reduced paracellular transmigration by reducing the levels of reactive oxygen species (ROS), Src phosphorylation, and vascular endothelial-cadherin (VE-cadherin) phosphorylation. GBEE reduced transcellular migration via inhibition of Ras homolog family member A (RhoA) and Rho-associated protein kinase (ROCK) expression and phosphorylation of the ezrin-radixin-moesin (ERM) protein. Incubation of EA.hy926 cells with GBEE for 8 h and stimulation with TNF-α for 3 h reduced the phosphorylation of the inhibitor of kappa B (IĸB) and DNA-binding activity of nuclear factor-ĸB (NF-ĸB). These results suggest that GBEE has a protective effect against endothelial dysfunction via suppression of leukocyte-endothelium adhesion and transmigration.