2002 Fiscal Year Final Research Report Summary
Detection of Doxirubicin Induced Mycardial cell injury using Monoclonal Antibodies for Myocardial Annexin V
Project/Area Number |
13670969
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Radiation science
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Research Institution | Tokyo Women's Medical University |
Principal Investigator |
KOBAYASHI Hideki Tokyo Woman's Medical University, Dept of Rodilolos, 医学部, 講師 (10178329)
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Co-Investigator(Kenkyū-buntansha) |
KUSAKABE Kiyoko Tokyo Woman's Medical University, Dept of Rodilolos, 医学部, 教授 (80075473)
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Project Period (FY) |
2001 – 2002
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Keywords | anti-Annexin V antibody / imaging / 抗体イメージング / アドリアマイシン心筋症 / 早期発見 |
Research Abstract |
Detection of Doxirubicin Induced Mycardial cell injury using Monoclonal Antibodies for Myocardial Annexin V Annex in V, a calcium-dependent phospholipid-binding protein that exists in the soluble fraction of myocardium, was translocated from the soluble fraction of myocardium to the myocardial cell membrane when the myocardium was damaged in the patients with congestive heart failure. The purpose of this sturdy was to clarify the diagnostic value of In-111 labeled Monoclonal Antibodies for Myocardial Annexin V for the detection of damaged myocardium. Methods. Forty Wister rats were injected 0.2mg of doxirubicin weekly for making doxirubicin induced cardiomyopathy model. In-111 labeled anti-Annexin V antibody was injected 4, 6, 8 and 9 weeks after the doxirubicin Injection. Results. Heart/Lung ratio in doxirubicin group on weeks 4, 6, 8 and 9 weeks (2.56±0.48, 2.30±0.49, 2.20±0.23, 0.85±0.41) were significantly higher than that in control group (1.30±0.21, 1.32±0.38, 1.39±0.23). Biodistribution analysis also showed that In-111 labeled anti-Annexin V antibody accumulation was higher in doxirubicin group than that in control group. Conclusion. In-111 labeled anti-Annexin V antibody scintigraphy positively imaged damaged myocardium in doxirubicin induced rat cardiomyopathy model.
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