Acid increases PGE 2 in the duodenal mucosa in rats

• Published in: Journal of clinical biochemistry and nutrition 2022-01, Vol.70 (1), p.28
• Main Authors: Fujimura, Tadahiro, Kondo, Takashi, Kobayashi, Kimiko, Duan, Shaoqi, Kanda, Hirosato, Kono, Tomoaki, Fukushima, Masashi, Tomita, Toshihiko, Oshima, Tadayuki, Fukui, Hirokazu, Fujii, Yoshihito, Konemura, Takashi, Okada, Hiroki, Yamanaka, Hiroki, Dai, Yi, Noguchi, Koichi, Miwa, Hiroto
• Format: Article
• Language: English
• ISSN: 0912-0009

Attention has recently been paid to the duodenum as the pathophysiologic center of functional dyspepsia. However, the precise mechanisms of symptom generation remain unknown. We here investigated the effect of acid on duodenal prostaglandin E and localization of prostaglandin E related receptors. Sprague-Dawley rats were used for this study. Hydrochloric acid was administered in the duodenum, then prostaglandin E levels in the duodenum were measured using the ELISA. The expression and localization of prostaglandin receptors (EP1-4) and the mRNAs of prostaglandin synthases were investigated using hybridization histochemistry in duodenal tissue. After acid perfusion, prostaglandin E levels in the duodenum significantly increased. EP3 was expressed mainly at the myenteric plexus in the duodenal mucosa, and EP4 at both the epithelial surface and myenteric plexus. Contrary, EP2 was sparsely distributed in the villi and EP1 were not clearly seen on hybridization histochemistry. Prostaglandin-synthetic enzymes were also distributed in the duodenal mucosa. The prostaglandin E levels in the duodenum increased after acidification. Prostaglandin E receptors and prostaglandin E -producing enzymes were both observed in rat duodenum. These observations suggest that duodenal prostaglandin E possibly play a role in the symptom generation of functional dyspepsia.