YS 49, a Synthetic Isoquinoline Alkaloid, Protects Sheep Pulmonary Artery Endothelial Cells from tert-butylhydroperoxide-mediated Cytotoxicity.
- Author:
Won Seog CHONG
1
;
Sun Young KANG
;
Young Jin KANG
;
Min Kyu PARK
;
Young Soo LEE
;
Hye Jung KIM
;
Han Geuk SEO
;
Jae Heun LEE
;
Hye Sook YUN-CHOI
;
Ki Churl CHANG
Author Information
1. Department of Pharmacology, College of Medicine, and Institute of Health Science, Gyeongsang National University, Jinju, Korea. kcchang@gsnu.ac.kr
- Publication Type:Original Article
- Keywords:
Reactive oxygen species;
Sheep pulmonary artery endothelial cells;
Heme oxygenase;
YS 49;
Antioxidant
- MeSH:
Apoptosis;
Cell Survival;
Endothelial Cells*;
Endothelium;
Heme Oxygenase (Decyclizing);
Lipid Peroxidation;
Pulmonary Artery*;
Reactive Oxygen Species;
Sheep*;
Zinc
- From:The Korean Journal of Physiology and Pharmacology
2005;9(5):283-289
- CountryRepublic of Korea
- Language:English
-
Abstract:
Endothelium, particularly pulmonary endothelium, is predisposed to injury by reactive oxygen species (ROS) and their derivatives. Heme oxygenase (HO) has been demonstrated to provide cytoprotective effects in models of oxidant-induced cellular and tissue injuries. In the present study, we investigated the effects of YS 49 against oxidant [tert-butylhydroperoxide (TBH) ]-induced injury using cultured sheep pulmonary artery endothelial cells (SPAECs). The viability of SPAECs was determined by quantifying reduction of a fluorogenic indicator Alamar blue. We found that TBH decreased cell viability in a time- and concentration-dependent manner. YS 49 concentration- and time-dependently increased HO-1 induction on SPAECs. As expected, YS 49 significantly decreased the TBH-induced cellular injury. In the presence of zinc protophorphyrin, HO-1 inhibitor, effect of YS 49 was significantly inhibited, indicating that HO-1 plays a protective role for YS 49. Furthermore, YS 49 showed free radical scavenging activity as evidenced by 1, 1-diphenyl-2-picrylhydrazyl (DPPH) and inhibition of lipid peroxidation. However, YS 49 did not inhibit apoptosis induced by lipopolysaccharide (LPS) in SPAECs. Taken together, HO-1 induction along with strong antioxidant action of YS 49 may be responsible for inhibition of TBH-induced injury in SPAECs.
