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

Journal of Pharmacological Sciences

Hiroyuki Nishikawa¹  Sachiyo Nishimura¹  Atsufumi Kawabata¹  Yuka Terada¹  Mayuko Fujimura¹  Fumiko Sekiguchi¹  Maho Tsubota¹ 

[1] Division of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, Japan

关键词: transient receptor potential ankyrin-1 (TRPA1);    proteinase-activated receptor-2 (PAR2);    pancreatic pain;   

DOI  :  10.1254/jphs.13128SC

学科分类：药学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(13)Cited-By(4)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.

【 授权许可】

Unknown