<p>Postoperative adhesions frequently occur following abdominal surgical interventions, leading to serious morbidities and requiring new therapeutic strategies. The development of new therapeutic agents to reduce postoperative adhesions needs animal models that closely mirror human pathophysiology. In this study, we established a novel surgical adhesion model in cynomolgus monkeys, which are characteristically similar to humans. Our model reliably and reproducibly developed adhesions. Histopathological analyses revealed that monkeys undergoing our novel surgery method exhibited changes consistent with those in monkeys that underwent open abdominal surgery. Furthermore, the cellular components of the adhesion tissue in our monkey model reflected those reported in human adhesion tissue. Furthermore, time-course transcriptomic analyses showed that our model accurately recapitulates the well-known progression cascade of postoperative adhesions. In addition, it identified the upregulation of gene that is absent in rodents. We expect our novel surgical method to be a promising tool for elucidating the detailed biology of postoperative adhesions and for assessing new therapeutic treatments with high translatability to human biology.</p>

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Development of a novel postoperative adhesion induction model in cynomolgus monkeys with high reliability and reproducibility

  • Kenji Nakagawa,
  • Masaki Yamazaki,
  • Hiromi Tanimura,
  • Narumi Sakaguchi,
  • Miho Kohara,
  • Izumi Sato,
  • Masahiro Azuma,
  • Ayako Nishimoto-Kakiuchi,
  • Atsuhiko Kato,
  • Takehisa Kitazawa,
  • Ryo Konno,
  • Tadashi Sankai

摘要

Postoperative adhesions frequently occur following abdominal surgical interventions, leading to serious morbidities and requiring new therapeutic strategies. The development of new therapeutic agents to reduce postoperative adhesions needs animal models that closely mirror human pathophysiology. In this study, we established a novel surgical adhesion model in cynomolgus monkeys, which are characteristically similar to humans. Our model reliably and reproducibly developed adhesions. Histopathological analyses revealed that monkeys undergoing our novel surgery method exhibited changes consistent with those in monkeys that underwent open abdominal surgery. Furthermore, the cellular components of the adhesion tissue in our monkey model reflected those reported in human adhesion tissue. Furthermore, time-course transcriptomic analyses showed that our model accurately recapitulates the well-known progression cascade of postoperative adhesions. In addition, it identified the upregulation of gene that is absent in rodents. We expect our novel surgical method to be a promising tool for elucidating the detailed biology of postoperative adhesions and for assessing new therapeutic treatments with high translatability to human biology.