The Korean Journal of Physiology and Pharmacology

The Korean Society of Pharmacology (대한약리학회)
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YS 49, a Synthetic Isoquinoline Alkaloid, Protects Sheep Pulmonary Artery Endothelial Cells from tert-butylhydroperoxide-mediated Cytotoxicity

  • Chong, Won-Seog (Department of Pharmacology, College of Medicine, Seonam University) ;
  • Kang, Sun-Young (Department of Pharmacology, College of Medicine, and Institute of Health Science, Gyeongsang National University) ;
  • Kang, Young-Jin (Department of Pharmacology, College of Medicine Yeungnam University) ;
  • Park, Min-Kyu (Department of Pharmacology, College of Medicine, and Institute of Health Science, Gyeongsang National University) ;
  • Lee, Young-Soo (Department of Pharmacology, College of Medicine, and Institute of Health Science, Gyeongsang National University) ;
  • Kim, Hye-Jung (Department of Pharmacology, College of Medicine, and Institute of Health Science, Gyeongsang National University) ;
  • Seo, Han-Geuk (Department of Pharmacology, College of Medicine, and Institute of Health Science, Gyeongsang National University) ;
  • Lee, Jae-Heun (Department of Pharmacology, College of Medicine, and Institute of Health Science, Gyeongsang National University) ;
  • ChoiYun, Hye-Sook (Natural Products Research Institute, Seoul National University) ;
  • Chang, Ki-Churl (Department of Pharmacology, College of Medicine, and Institute of Health Science, Gyeongsang National University)
  • Published : 2005.10.21
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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 timeand 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.

Keywords

References

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