2-B-P-033 〇鎌内 朋子¹、村田 幸久²、有竹 浩介³ Tomoko Kamauchi¹, Takahisa Murata², Kosuke Aritake^{3 1}第一薬科大・薬・薬剤設計、²東京大・院農学生命科学・放射線動物科学、³第一薬科大・薬・薬品作用 ¹Lab. Ind. Pharmacol. Daiichi Univ. Pharm., ²Dept. Anim. Radiology, Univ. of Tokyo, ³Lab. Chem. Pharmacol. Daiichi Univ. Pharm. Delayed wound healing is a major problem in patients with diabetes, which significantly impairs their quality of life. Prostaglandin (PG) D₂ is a major inflammatory lipid mediator synthesized by hematopoietic PGD₂ synthase (HPGDS) from PGH₂, a common precursor of all of PGs. We have previously shown that HPGDS produced PGD₂ is involved in delayed wound healing in diabetic skin. In this study, we investigated the involvement of DP1 receptor in cutaneous wound healing in streptozotocin (STZ)-induced diabetic mice. C57BL/6 mice were injected intraperitoneal with 50 mg/kg of STZ daily for 5 days. Four weeks after the injection of STZ, a full thickness wound was created with an 8-mm diameter biopsy punch on the dorsal of mice. Wound healing was significantly decelerated in diabetic mice compared with non-diabetic mice. HPGDS mRNA was significantly increased in diabetic mouse skin compared to nondiabetic mouse skin. On the other hand, there was no significant change in the amount of DP1 receptor mRNA. Furthermore, immunohistochemically analysis revealed that HPGDS was expressed in epidermal Langerhans cells of diabetic mice, and the DP1 receptor was expressed in keratinocytes. These results suggest that in hyperglycemic skin, PGD₂ produced by Langerhans cells acts on DP1 receptors on keratinocytes and may be involved in delayed wound healing.