Journal of Society of Preventive Korean Medicine (대한예방한의학회지)

Society of Preventive Korean Medicine (대한예방한의학회)
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Effects of Demethoxycurcumin Isolated from Radix Curcumae on Arterial Restenosis in Rats

울금(鬱金)에서 분리된 demethoxycurcumin이 백서의 혈관재협착에 미치는 효과

  • Kil, In-Ho (Dept. of Preventive Oriental Medicine, College of Oriental Medicine, Wonkwang University) ;
  • Chong, Myong-Soo (Dept. of Preventive Oriental Medicine, College of Oriental Medicine, Wonkwang University) ;
  • Shin, Chang-Ho (Dept. of the Third Medicine, Professional Graduate School of Oriental Medicine, Wonkwang University) ;
  • Pae, Hyun-Ock (Dept. of Microbiology and Immunology, College of Medicine, Wonkwang University) ;
  • Chung, Hun-Taeg (Dept. of Microbiology and Immunology, College of Medicine, Wonkwang University) ;
  • Lee, Ki-Nam (Dept. of the Third Medicine, Professional Graduate School of Oriental Medicine, Wonkwang University)
  • 길인호 (원광대학교 한의과대학 예방의학교실) ;
  • 정명수 (원광대학교 한의과대학 예방의학교실) ;
  • 신창호 (원광대학교 한의학전문대학원 제3의학과) ;
  • 배현옥 (원광대학교 의과대학 미생물면역학교실) ;
  • 정헌택 (원광대학교 의과대학 미생물면역학교실) ;
  • 이기남 (원광대학교 한의학전문대학원 제3의학과)
  • Published : 2008.12.31
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Abstract

The pathobiologic process of arterial stenosis following balloon angioplasty continues to be an enigmatic problem in clinical settings. This study investigates the ability of demethoxycurcumin, a curcuminoid isolated from Radix Curcumae, to attenuate balloon injury-induced neointima(NI) formation in the rat carotid artery. It was found that demethoxycurcumin induced inducible heme oxygenase(HO-1) expression and inhibited dose-dependently cellular proliferation in rat vascular smooth muscle cells. Perivascular application of demethoxycurcumin immediately following injury significantly reduced NI area and NI thickness 2 weeks post-injury. Interestingly, treatment with tin-protoporphyrin IX, a HO inhibitor, reversed the effects of demethoxycurcumin on NI formation. These results implicate demethoxycurcumin as a potent new therapeutic agent that is capable of reducing post-angioplasty arterial stenosis through induction of the HO-1 expression.

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