Scheiman J M, Kraus E R, Boland C R
Research Service, Veterans Administration Medical Center, Ann Arbor, Michigan.
Gastroenterology. 1992 Dec;103(6):1842-50. doi: 10.1016/0016-5085(92)91443-8.
Key components of the mucous gel include the glycoprotein mucin and surface-active phospholipids. In the present study, mucin production and release of the surface-active phospholipid phosphatidylcholine (PC) into the medium were measured with an isolated canine mucous cell culture system. Stimulation of glycoprotein synthesis in response to 10(-4) mol/L histamine (160% +/- 9% of control, P < 0.01), 10(-6) mol/L gastrin (129% +/- 7%, P < 0.01), and 10(-6) mol/L carbamylcholine (129% +/- 7%, P < 0.01) was observed by metabolic labeling, whereas prostaglandin E2 (PGE2) had no effect. The effect of histamine was blocked by the H2 receptor antagonist cimetidine but not the H1 receptor antagonist diphenhydramine (P < 0.01). Activators of adenylate cyclase and cyclic adenosine monophosphate analogs significantly stimulated mucin synthesis (P < 0.05). A 7.8% +/- 1.7% increase in mucin above basal levels after 24 hours was observed with a solid-phase immunoassay in control wells, whereas histamine, gastrin, and carbamylcholine increased total mucin by 14% +/- 0.7%, 17% +/- 4.3%, and 20.4% +/- 4%, respectively (all P < 0.01), and PGE2 had no significant effect. PC release was stimulated by the administration of histamine, carbamylcholine, gastrin (108%-110% of control, P < or = 0.05), and PGE2 (120% of control, P < 0.01). The acid secretagogues histamine, gastrin, and carbamylcholine stimulated mucin synthesis and PC release. PGE2 has no direct role in the synthesis of canine gastric mucin but stimulates release of surface-active phospholipids. The mechanisms responsible for acid secretion provide for the coordinated production of the primary layer of defense against the injurious effects of low pH.
黏液凝胶的关键成分包括糖蛋白黏蛋白和表面活性磷脂。在本研究中，使用分离的犬黏液细胞培养系统测量黏蛋白的产生以及表面活性磷脂磷脂酰胆碱（PC）向培养基中的释放。通过代谢标记观察到，10⁻⁴mol/L组胺（为对照的160%±9%，P<0.01）、10⁻⁶mol/L胃泌素（129%±7%，P<0.01）和10⁻⁶mol/L氨甲酰胆碱（129%±7%，P<0.01）刺激糖蛋白合成，而前列腺素E2（PGE2）无作用。组胺的作用被H2受体拮抗剂西咪替丁阻断，但未被H1受体拮抗剂苯海拉明阻断（P<0.01）。腺苷酸环化酶激活剂和环磷酸腺苷类似物显著刺激黏蛋白合成（P<0.05）。在对照孔中，通过固相免疫测定法观察到24小时后黏蛋白比基础水平增加7.8%±1.7%，而组胺、胃泌素和氨甲酰胆碱分别使总黏蛋白增加14%±0.7%、17%±4.3%和20.4%±4%（均P<0.01），且PGE2无显著作用。组胺、氨甲酰胆碱、胃泌素（为对照的108% - 110%，P≤0.05）和PGE2（为对照的120%，P<0.01）刺激PC释放。酸分泌剂组胺、胃泌素和氨甲酰胆碱刺激黏蛋白合成和PC释放。PGE2在犬胃黏蛋白合成中无直接作用，但刺激表面活性磷脂的释放。负责酸分泌的机制为抵御低pH损伤作用的初级防御层的协同产生提供了条件。
