Protective Effects of Dohongsamul-tang on Zinc-mediated Cytotoxicity in H9c2 Cardiomyoblast Cells

산화적 손상에 의해 유발된 심근세포 독성에 대한 도홍사물탕의 방어효과

  • You Bong Sun (Department of Internal Medicine, College of Oriental Medicine, Wonkwang University) ;
  • Jung Jae Eun (Department of Internal Medicine, College of Oriental Medicine, Wonkwang University) ;
  • Park Jin Young (Department of Internal Medicine, College of Oriental Medicine, Wonkwang University) ;
  • Yun Jong Min (Department of Internal Medicine, College of Oriental Medicine, Wonkwang University, Professional Graduate School of Oriental Medicine, Wonkwang University) ;
  • Lee In (Department of Internal Medicine, College of Oriental Medicine, Wonkwang University) ;
  • Moon Byung Soon (Department of Internal Medicine, College of Oriental Medicine, Wonkwang University, Professional Graduate School of Oriental Medicine, Wonkwang University)
  • 유봉선 (원광대학교 한의과대학 심계내과학교실) ;
  • 정재은 (원광대학교 한의과대학 심계내과학교실) ;
  • 박진영 (원광대학교 한의과대학 심계내과학교실) ;
  • 윤종민 (원광대학교 한의과대학 심계내과학교실, 원광대학교 한의학전문대학원) ;
  • 이인 (원광대학교 한의과대학 심계내과학교실) ;
  • 문병순 (원광대학교 한의과대학 심계내과학교실, 원광대학교 한의학전문대학원)
  • Published : 2004.10.01

Abstract

The water extract of Dohongsamul-tang(DHSMT)has been traditionally used for treatment of ischemic heart in oriental medicine. However, little is known about the mechanism by which the water extract of DHSMT rescues cells from these damages. Therefore, this study was designed to evaluate the protective effects of DHSMT on zinc-mediated cytotoxicity in H9c2 cardiomyoblast cells. This study demonstrates that treatment of H9c2 cells with zinc caused a decrease in cell viability in a dose dependent manner and a chromatin condensation. Zinc induced the cleavage of poly(ADP-ribose) polymerase (PARP). In addition, zinc induced the decrease of Bcl-2, as well as increase of Bak expression and mitochondrial dysfunction. Zinc-induced H9c2 cell death was remarkably prevented by the pretreatment of DHSMT with consistent suppression of the cleavage of poly(ADP-ribose) polymerase (PARP), mitochondrial dysfunction and the expression of Bak and Bcl-2. Taken together, the results suggest that zinc induced severe cell death in H9c2 cardiomyoblast cells via intracellular GSH(reduced glutathione) depletion and the protective effects of DHSMT against oxidative injuries may be achieved through modulation of mitochondrial dysfunction and scavenging of ROS(reactive oxygen species).

Keywords

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