摘要
背景:研究不同抗溃疡药物在防治应激性溃疡(SU)时,其对胃黏膜细胞学行为的作用是否有助于SU的防治。目的:观察抗溃疡药物奥美拉唑、米索前列醇和铝碳酸镁对SU的疗效,及其对细胞凋亡和与凋亡相关的细胞因子一氧化氮合酶(NOS)表达的影响。方法:水浸-束缚应激(WRS)结束后2h,计算胃黏膜损伤的溃疡指数(UI):原位末端标记(TUNEL)法检测胃黏膜细胞凋亡;免疫组化法检测神经型NOS(nNOS)和诱导型NOS(iNOS)表达的变化。结果:奥美拉唑(O)组、米索前列醇(M)组和铝碳酸镁(H)组胃黏膜损伤均较生理盐水组显著减轻(P<0.01),胃黏膜细胞凋亡发生率均显著降低(P<0 01),但O组和M组的效果优于H组。与生理盐水组比较,3组用药组的nNOS表达均显著增加(P<0.01),iNOS表达均显著降低(P<0.01),M组和H组的nNOS表达升高较O组更为显著(P<0.05)。结论:奥美拉唑、米索前列醇和铝碳酸镁作用于SU发生的不同环节,可显著抑制细胞凋亡的发生,对SU均有明显防治作用。寻找对细胞有直接保护作用的药物以提高细胞的抗应激能力可能是防治SU的最终途径。
Background: Whether the effects on cell behavior of gastric mucosa with different anti-ulcer drugs, which may be helpful for prevention and treatment of stress ulcer, are needed for investigation. Aims: To investigate the effects of anti-ulcer agents as omeprazole, misoprostol and hydrotalcite on stress ulcer, apoptosis and expression of apoptosis associated factor nitric oxide synthase (NOS). Methods: The mucosal injury was evaluated by ulcer index (UI), gastric mucosal apoptotic cells which were quantitated by terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) techniques while the expression of neural NOS (nNOS) and inducible NOS (iNOS) were detected by im-munohistochemical staining 2 hours after water-immersion and restraint stress (WRS). Results: In comparison with the saline group, the groups of pretreated omeprazole, misoprostol and hydrotalcite showed a significant reduction of damaged mucosa and epithelial cell apoptosis (P<0.01), and the effects of omeprazole and misoprostol were better than that of hydrotalcite. All the three anti-ulcer agents could increase the nNOS expression and decrease the iNOS expression (P<0.01), the effects of misoprostol and hydrotalcite on increase of expression of nNOS were better than that of omeprazole (P<0.05). Conclusions: Omeprazole, misoprostol and hydrotalcite act on different links of stress ulcer formation. These drugs inhibit apoptosis of gastric mucosal epithelial cells, and have anti stress effect. It may be the ultimate way for agents to prevent and cure stress ulcer by exerting the cytoprotective effect directly to improve the cell ability for countering stress injury.
出处
《胃肠病学》
2003年第1期11-14,共4页
Chinese Journal of Gastroenterology
基金
本课题由"十五"全军医药科研基金重点项目(01Z059)资助
