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Potential of HMGB-inhibitory oligodeoxynucleotide ISM ODN to neutrophil recruitment in mouse model of hepatitis.
Inoue, Asuka; Chiba, Shiho; Eto, Shotaro; Taniguchi, Tadatsugu; Yanai, Hideyuki.
Afiliação
  • Inoue A; Department of Inflammology, Research Center for Advanced Science and Technology (RCAST), The University of Tokyo, Tokyo, Japan.
  • Chiba S; Department of Inflammology, Research Center for Advanced Science and Technology (RCAST), The University of Tokyo, Tokyo, Japan.
  • Eto S; Department of Inflammology, Research Center for Advanced Science and Technology (RCAST), The University of Tokyo, Tokyo, Japan.
  • Taniguchi T; Department of Inflammology, Research Center for Advanced Science and Technology (RCAST), The University of Tokyo, Tokyo, Japan.
  • Yanai H; Department of Inflammology, Research Center for Advanced Science and Technology (RCAST), The University of Tokyo, Tokyo, Japan.
Genes Cells ; 28(3): 202-210, 2023 Mar.
Article em En | MEDLINE | ID: mdl-36550748
High-mobility group box 1 (HMGB1) is a nucleotide-binding chromatin protein that has also been characterized as a prototypical damage-associate molecular pattern. It triggers inflammatory responses upon release from damaged or dying cells. In fact, HMGB1 has been linked to the induction of many inflammatory diseases through immune cell activation including neutrophil recruitment. In this study, we examined the impact of HMGB1-binding inhibitory oligodeoxynucleotide (ISM ODN) on the development of hepatitis using a murine model of the disease. Our results indicate that ISM ODN effectively suppresses pathological features of hepatitis, including neutrophil accumulation. This study therefore may offer clinical insight into the treatment of hepatitis and possibly other inflammatory diseases.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Proteína HMGB1 / Hepatite Limite: Animals Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Proteína HMGB1 / Hepatite Limite: Animals Idioma: En Ano de publicação: 2023 Tipo de documento: Article