Contribution of TRPA1 as a Downstream Signal of Proteinase-Activated Receptor-2 to Pancreatic Pain

DOI Web Site Web Site PubMed 被引用文献2件 参考文献13件
  • Terada Yuka
    Division of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, Japan
  • Fujimura Mayuko
    Division of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, Japan
  • Nishimura Sachiyo
    Division of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, Japan
  • Tsubota Maho
    Division of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, Japan
  • Sekiguchi Fumiko
    Division of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, Japan
  • Nishikawa Hiroyuki
    Division of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, Japan
  • Kawabata Atsufumi
    Division of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, Japan

この論文をさがす

抄録

We examined if TRPA1, like TRPV1, contributes to pancreatic nociceptor excitation following proteinase-activated receptor-2 (PAR2) stimulation and to pancreatitis-related pain in mice. A PAR2-activating peptide, infused into the pancreatic duct, caused spinal Fos expression, which was prevented by AP18, a TRPA1 inhibitor. Repeated administration of cerulein caused referred hyperalgesia accompanying pancreatitis, which was reversed by SB366791, a TRPV1 inhibitor, but not AP18. AP18, administered in combination with a subeffective dose of SB366791, significantly suppressed the referred hyperalgesia. Our findings suggest that TRPA1, like TRPV1, mediates PAR2-triggered pancreatic nociception and that TRPA1 in collaboration with TRPV1 latently contributes to pancreatitis-related pain.

収録刊行物

被引用文献 (2)*注記

もっと見る

参考文献 (13)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ