Pathological Study for Peptic Ulcer-Role of Prostaglandin

研究了甘草素（PGs）在胃粘膜中的作用。首先，采用离体组织培养法研究了大鼠离体胃壁PGs的释放。PGI_2的释放量以塞曲林侧为高。相反，粘膜侧的PGE 2释放较高。PGs的释放在高钙培养基中增加，并随着EGTA的加入而减少。结果提示，PGE_2和PGI_2在大鼠胃壁不同层合成，胃内PGs的合成和释放可能需要钙离子的参与。组胺和tetragastrin均能剂量依赖性地增加胃粘膜中PGE_2的含量，并能显著地预防0.6N HCL引起的胃粘膜损伤。吲哚美辛预处理可消除这些作用。这些结果表明，促分泌素，如组胺或tetragastrin通过增加内源性PGE 2保护胃粘膜。其次，用免疫组化方法观察了大鼠胃粘膜中PGE_2产生细胞的分布，发现PGE_2阳性细胞主要分布于胃粘膜上皮细胞的腔面和壁细胞的胞浆中。提示大鼠胃粘膜壁细胞主要合成PGE_2。第三，在离体大鼠胃表面上皮细胞中检测乙醇引起的损伤和16，16-二甲基PGE_2对其的预防作用。乙醇引起的细胞损伤呈剂量依赖性，16，16-二甲基前列腺素E2可明显抑制15%乙醇引起的细胞损伤。提示16，16-二甲基前列腺素E_2对胃粘膜细胞有直接的保护作用。

The role of prostaglandins (PGs ) in the gastric mucosa was investigated. Firstly, the release of PGs from the isolated gastric wall of rats was investigated by a tissue incubation method in vitro. The release of PGI2 was higher on the serosal side. The release of PGE2 was, in contrast, higher on the mucosal side. Release of PGs increased in a high calcium medium, and decreased with the addition of EGTA. These results suggest that PGE2 and PGI2 are synthesized in different layers of the gastric wall, and that calcium ion may be required for synthesis or release of PGs in rat stomach. The PGE2 level in the gastric mucosa was increased by histamine or tetragastrin in a dose- related way, and they significantly prevented the gastric mucosal damage caused by 0.6N HCL. These effects were abolished by the pretreatment of indomethacin. These results suggest that secretagogues such as histamine or tetragastrin through increasing endogenous PGE2 protect the gastric mucosa. Secondly, cellular localization of PGE2 producing cells were investigated by the immunoperoxidase technique in rat gastric mucosa.Positive stainings for PGE2 were observed on the luminal surface of the surface epithelial cells and in the cytoplasm of the parietal cells in the deeper layers of the mucosa. These results suggest that parietal cells mainly synthesize PGE2 in rat gastric mucosa. Thirdly, damage caused by ethanol and its prevention by 16,16-dimethyl PGE2 were tested in surface epithelial cells isolated from rat stomach in vitro. Ethanol caused cell damage in a dose-related way, and 16,16-dimethyl PGE2 significantly inhibited the damage caused by 15% ethanol. These results suggest that 16,16-dimethyl PGE2 has direct protective effect on gastric cells.