Effect of arazyme on the lipopolysaccharide‑induced inflammatory response in human endothelial cells.
Arazyme is a novel extracellular metalloprotease secreted by Aranicola proteolyticus. Endothelial cells are involved in the pathogenesis of a number of inflammatory diseases, induce uncontrolled cell viability and express various inflammatory mediators, including cytokines, chemokines, adhesion molecules and reactive oxygen species (ROS). In the current study, human umbilical vein endothelilal cells (HUVECs) were used to investigate the anti‑inflammatory effects of arazyme following lipopolysaccharide (LPS) stimulation. Apoptosis of HUVECs due to LPS was inhibited by arazyme. In various inflammatory responses induced by LPS, arazyme inhibited the secretion of the monocyte chemoattractant protein‑1 and interleukin‑6, and the expression of vascular cell adhesion molecule‑1 and intercellular adhesion molecule‑1. Arazyme also suppressed ROS production in HUVECs. The action of arazyme was not associated with NF‑κB activity in HUVECs. These results indicate that arazyme has anti‑inflammatory properties in inflamed endothelial cells and may be useful as a therapeutic agent for inflammatory diseases associated with endothelial cells.
Department of Biomedical Laboratory Science, School of Medicine, Eulji University, Daejeon 301‑746, Republic of Korea.
In Sik
IS
Kim
Department of Clinical Laboratory Science, College of Health and Therapy, Daegu Hanny University, Gyeongsan 712‑715, Republic of Korea.
Eun Ju
EJ
Yang
Insect Biotech Co., Ltd., Dajeon 305‑811, Republic of Korea.
Dong-Ha
DH
Shin
Industrial Bio‑Material Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305‑806, Republic of Korea.
Kwang-Hee
KH
Son
Industrial Bio‑Material Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305‑806, Republic of Korea.
Ho-Yong
HY
Park
Department of Clinical Laboratory Science, Wonkwang Health Science University, Iksan, Chonbuk 570‑750, Republic of Korea.
Ji-Sook
JS
Lee
D017209:Apoptosis / Q000187:drug effects*; D018932:Chemokine CCL2 / Q000378:metabolism; D004755:Enterobacteriaceae / Q000201:enzymology; D015870:Gene Expression / Q000187:drug effects; D061307:Human Umbilical Vein Endothelial Cells; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity; D045726:Metalloproteases / Q000302:isolation & purification / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
D018932:Chemokine CCL2; D015850:Interleukin-6; D008070:Lipopolysaccharides; D017382:Reactive Oxygen Species; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D045726:Metalloproteases