Prostaglandin E2 release in gastric antral mucosa of guinea‐pigs: basal PGE2 release by cyclo‐oxygenase 2 and ACh‐stimulated PGE2 release by cyclo‐oxygenase 1
Prostaglandin E2 release in gastric antral mucosa of guinea‐pigs: basal PGE2 release by cyclo‐oxygenase 2 and ACh‐stimulated PGE2 release by cyclo‐oxygenase 1
复制标题
豚鼠胃窦粘膜中前列腺素 E2 的释放：环加氧酶 2 的基础 PGE2 释放和环加氧酶 1 的乙酰胆碱刺激的 PGE2 释放
作者：
C. Shimamoto;Yoshihiko Nakanishi;K. Katsu;T. Nakano;T. Kubota;H. Mori;T. Nakahari
前列腺素 E2 (PGE2) 由环加氧酶的两种亚型（COX1 和 COX2）产生，是胃粘膜防御的关键介质。在本研究中，将豚鼠的胃窦粘膜与各种激动剂或拮抗剂一起在培养基中孵育，并使用 PGE2 EIA 试剂盒测量 PGE2 浓度。前列腺素 E2 从胃窦粘膜自发释放（基础 PGE2 释放），乙酰胆碱（ACh，10 μm）通过细胞内 Ca2+ 浓度 ([Ca2+]i) 介导增强 PGE2 释放（ACh 刺激的 PGE2 释放）。花生四烯酸可增强两种形式的 PGE2 释放，而磷脂酶 A2 抑制剂（戊基肉桂酰邻氨基苯甲酸）和 COX 抑制剂（乙酰水杨酸和吲哚美辛）可减少它们。 5-(4-氯苯基)-1-(4-甲氧基苯基)-3-三氟甲基吡唑（SC560，100 nm，COX1 选择性抑制剂）抑制 ACh 刺激的 PGE2 释放，但基础 PGE2 释放没有任何减少。 N-(2-环己氧基-4-硝基苯基)甲磺酰胺（NS398，20 μm，一种 COX2 选择性抑制剂）可减少基础 PGE2 释放，但不会减少 ACh 刺激的 PGE2 释放。然而，在 SC560 或 NS398 存在的情况下，离子霉素（一种 Ca2+ 离子载体）会增加胃窦粘膜的 PGE2 释放，表明 COX1 和 COX2 受 [Ca2+]i 调节。这些发现表明，含有 COX1 的细胞具有 ACh 受体，但含有 COX2 的细胞则没有。此外，在分离的胃窦上皮细胞中，SC560 减少了基础和 ACh 刺激的 PGE2 释放，但 NS398 没有。总之，在胃窦粘膜中，基础 PGE2 释放主要由非上皮细胞的 COX2 维持，ACh 刺激的 PGE2 释放由上皮细胞的 COX1 维持。
Prostaglandin E2 (PGE2), which is generated by two isoforms of cyclo‐oxygenase (COX1 and COX2), is a key mediator in gastric mucosal defense. In the present study, antral mucosa of guinea‐pigs was incubated with various agonists or antagonists in a medium, the PGE2 concentration of which was measured using a PGE2 EIA kit. Prostaglandin E2 was released from the antral mucosa spontaneously (basal PGE2 release) and acetylcholine (ACh, 10 μm) enhanced the PGE2 release (ACh‐stimulated PGE2 release) was mediated via intracellular Ca2+ concentration ([Ca2+]i). Arachidonic acid enhanced both forms of PGE2 release, and a phospholipase A2 inhibitor (amylcinnamoyl anthranilic acid) and COX inhibitors (acetylsalicylic acid and indomethacin) decreased them. 5‐(4‐Chlorophenyl)‐1‐(4‐methoxyphenyl)‐3‐trifluoromethylpyrazol (SC560, 100 nm, a COX1‐selective inhibitor) inhibited ACh‐stimulated PGE2 release without any decrease in basal PGE2 release. N‐(2‐Cyclohexyloxy‐4‐nitrophenyl) methanesulphonamide (NS398, 20 μm, a COX2‐selective inhibitor) decreased basal PGE2 release without any reduction of ACh‐stimulated PGE2 release. However, ionomycin (a Ca2+ ionophore) increased PGE2 release from antral mucosa in the presence of SC560 or NS398, suggesting that COX1 and COX2 are regulated by [Ca2+]i. These findings indicate that COX1‐containing cells have ACh receptors but COX2‐containing cells do not. Moreover, in isolated antral epithelial cells, SC560 decreased basal and ACh‐stimulated PGE2 release, but NS398 did not. In conclusion, in antral mucosa, basal PGE2 release is mainly maintained by COX2 of non‐epithelial cells, and ACh‐stimulated PGE2 release is maintained by COX1 of epithelial cells.
影响因子：
7.7
作者：
Robertson, RP
通讯作者：
Robertson, RP
致密黄斑：最新进展。
影响因子：
4.9
作者：
Harris,RC
通讯作者：
Harris,RC