Henagan J M, Smith G S, Schmidt K L, Miller T A
Ann Surg. 1986 Dec;204(6):698-704. doi: 10.1097/00000658-198612000-00014.
The role of barrier mucus in mediating the protective effects of 16,16 dimethyl PGE2 (dm PGE2) against ethanol-induced gastric injury, with and without concomitant treatment with N-acetyl-cysteine (NAC), a potent mucolytic agent, was evaluated. Fasted rats were orally administered either saline, 10 micrograms/kg dm PGE2, 20% NAC, or 10 micrograms/kg dm PGE2 plus 20% NAC. In the first study, the rats were killed 15 minutes later and their stomachs were removed and assayed for barrier mucus adherent to the gastric wall using the Alcian blue technique. In the second study, the rats were orally given 2 mL of absolute ethanol (EtOH) after receiving one of these pretreatment regimens, and 5 minutes later they were killed and their stomachs were evaluated histologically by light microscopy for the magnitude of EtOH injury. Although NAC significantly reduced the thickness of barrier mucus by 76% when compared with control animals, it did not adversely affect the ability of dm PGE2 to spare the deep epithelium from injury by EtOH. In fact, NAC was as effective a protective agent as dm PGE2. Neither agent prevented damage to the surface epithelium by EtOH, verifying previous studies regarding the protective effects of prostaglandins. These results indicate that both dm PGE2 and NAC prevent EtOH-induced damage to the deeper layers of the gastric mucosa independent of mucus gel layer thickness, suggesting that other mechanisms than mucus are involved in mediating this protection.
评估了屏障黏液在介导16,16 - 二甲基前列腺素E2（dm PGE2）对乙醇诱导的胃损伤的保护作用中的角色，其中有无同时使用强力黏液溶解剂N - 乙酰半胱氨酸（NAC）。空腹大鼠分别口服生理盐水、10微克/千克dm PGE2、20% NAC或10微克/千克dm PGE2加20% NAC。在第一项研究中，15分钟后处死大鼠，取出胃，使用阿尔新蓝技术检测附着在胃壁上的屏障黏液。在第二项研究中，在接受上述预处理方案之一后，给大鼠口服2毫升无水乙醇（EtOH），5分钟后处死大鼠，通过光学显微镜对其胃进行组织学评估，以确定EtOH损伤的程度。尽管与对照动物相比，NAC显著降低了屏障黏液厚度达76%，但它并未对dm PGE2保护深层上皮免受EtOH损伤的能力产生不利影响。事实上，NAC作为一种保护剂与dm PGE2一样有效。两种药物均未预防EtOH对表面上皮的损伤，这证实了先前关于前列腺素保护作用的研究。这些结果表明，dm PGE2和NAC均可预防EtOH诱导的胃黏膜深层损伤，且与黏液凝胶层厚度无关，这表明除黏液外，其他机制也参与介导这种保护作用。
