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胃蛋白酶是否具有适应性细胞保护作用,尚不清楚。本工作观察了胃蛋白酶对牛磺胆酸所致的胃粘膜损伤的影响。酸性牛磺胆酸80mM 给禁食大鼠灌胃,90min 后可引起严重的胃粘膜损伤。胃蛋白酶225单位(U)溶于水、150U 溶于0.1N HCl 或75U 溶于0.2N HGl,三者分别作为“弱刺激”提前15min 灌胃,均可防止由牛磺胆酸所致胃粘膜的损伤;这种保护作用呈明显的量效关系,并可持续约90min 之久。消炎痛(一种前列腺素合成酶的抑制剂) 提前60min 皮下注射,可阻断胃蛋白酶的适应性细胞保护作用,如果皮下给予外源性前列腺素 E_2(PGE_2),则能使这一作用重新恢复。这些结果说明,弱的胃蛋白酶刺激具有对胃粘膜的适应性细胞保护作用,其产生机制可能是通过诱发内源性 PG 的合成和释放而实现的。
Whether pepsin has an adaptive cytoprotective effect is not clear. This work observed the effect of pepsin on gastric mucosal injury induced by taurocholic acid. Acidic taurocholic acid 80mM to the fasting gavage, 90min can cause severe gastric mucosal injury. Pepsin 225 units (U) dissolved in water, 150U dissolved in 0.1N HCl or 75U dissolved in 0.2N HGl, respectively, as three “weak stimulation” 15min prior to intragastric administration, can be prevented by taurocholate gastric mucosa Of the damage; this protective effect was significant dose-effect relationship, and sustainable for about 90min. Indomethacin, an inhibitor of prostaglandin synthase, subcutaneously injected 60 min earlier, blocks the adaptive cytoprotective effect of pepsin and, if subcutaneously administered with exogenous prostaglandin E 2 (PGE 2), reactivates this effect restore. These results indicate that weak pepsin stimulation has an adaptive cytoprotective effect on gastric mucosa, which may be caused by inducing the synthesis and release of endogenous PG.