Evaluating the potential of a new isotope-labelled glyco-ligand for estimating the remnant liver function of schistosoma-infected mice

P. C. Cheng, P. F. Chiang, K. M. Lee, C. H. Yeh, K. L. Hsu, S. W. Liu, L. H. Shen, C. L. Peng, C. K. Fan, T. Y. Luo

研究成果: 雜誌貢獻文章

6 引文 (Scopus)

摘要

A new glyco-derivative compound (OCTAM) was developed and labelled with isotope to form 188Re-OCTAM as a candidate nuclear medicine imaging agent for testing the liver function. We evaluated the potential of isotope-labelled OCTAM for estimating the remnant liver function in vitro and in vivo schistosoma-infected mice. The affinity of OCTAM to liver asialoglycoprotein receptors (ASGPR) was assessed by competitive inhibition assay in vitro. In vivo assessments were performed to score the remnant liver function in mice at different schistosomal infection stages. OCTAM binds specifically to ASGPR and showed competitive inhibition of anti-ASGPR antibody binding to hepatocytes, and was higher than that of other galactosyl ligands. Micro-SPECT/CT images of uninfected mice revealed strong liver uptake. Quantified serial images of mice infected for 9, 12 and 18 weeks showed delayed liver uptake, and the retention of uptake was inversely correlated with stage and grade of schistosoma infection. Pathological and biochemical analysis demonstrated that gradually accumulating liver injury caused by infection significantly influenced uptake of 188Re-OCTAM. Hepatic ASGPR expression diminished only in the chronic infection stage. This study demonstrated that the isotope-labelled OCTAM could accumulate in the liver, might have potential as an imaging agent for in vivo hepatic function evaluation of schistosomiasis.

原文英語
頁(從 - 到)129-139
頁數11
期刊Parasite Immunology
35
發行號3-4
DOIs
出版狀態已發佈 - 三月 2013

指紋

Schistosoma
Isotopes
Ligands
Asialoglycoprotein Receptor
Liver
Infection
Schistosomiasis
Nuclear Medicine
Hepatocytes

ASJC Scopus subject areas

  • Parasitology
  • Immunology

引用此文

Evaluating the potential of a new isotope-labelled glyco-ligand for estimating the remnant liver function of schistosoma-infected mice. / Cheng, P. C.; Chiang, P. F.; Lee, K. M.; Yeh, C. H.; Hsu, K. L.; Liu, S. W.; Shen, L. H.; Peng, C. L.; Fan, C. K.; Luo, T. Y.

於: Parasite Immunology, 卷 35, 編號 3-4, 03.2013, p. 129-139.

研究成果: 雜誌貢獻文章

Cheng, P. C. ; Chiang, P. F. ; Lee, K. M. ; Yeh, C. H. ; Hsu, K. L. ; Liu, S. W. ; Shen, L. H. ; Peng, C. L. ; Fan, C. K. ; Luo, T. Y. / Evaluating the potential of a new isotope-labelled glyco-ligand for estimating the remnant liver function of schistosoma-infected mice. 於: Parasite Immunology. 2013 ; 卷 35, 編號 3-4. 頁 129-139.
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abstract = "A new glyco-derivative compound (OCTAM) was developed and labelled with isotope to form 188Re-OCTAM as a candidate nuclear medicine imaging agent for testing the liver function. We evaluated the potential of isotope-labelled OCTAM for estimating the remnant liver function in vitro and in vivo schistosoma-infected mice. The affinity of OCTAM to liver asialoglycoprotein receptors (ASGPR) was assessed by competitive inhibition assay in vitro. In vivo assessments were performed to score the remnant liver function in mice at different schistosomal infection stages. OCTAM binds specifically to ASGPR and showed competitive inhibition of anti-ASGPR antibody binding to hepatocytes, and was higher than that of other galactosyl ligands. Micro-SPECT/CT images of uninfected mice revealed strong liver uptake. Quantified serial images of mice infected for 9, 12 and 18 weeks showed delayed liver uptake, and the retention of uptake was inversely correlated with stage and grade of schistosoma infection. Pathological and biochemical analysis demonstrated that gradually accumulating liver injury caused by infection significantly influenced uptake of 188Re-OCTAM. Hepatic ASGPR expression diminished only in the chronic infection stage. This study demonstrated that the isotope-labelled OCTAM could accumulate in the liver, might have potential as an imaging agent for in vivo hepatic function evaluation of schistosomiasis.",
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AU - Yeh, C. H.

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