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首页> 外文期刊>World Journal of Gastroenterology >Effects of nitric oxide on gastric ulceration induced by nicotine and cold-restraint stress
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Effects of nitric oxide on gastric ulceration induced by nicotine and cold-restraint stress

机译：一氧化氮对尼古丁诱发的胃溃疡及冷约束应激的影响

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AIM: Stress induces gastric ulceration in human and experimental animals. People tend to smoke more cigarettes when under stress. Nitric oxide (NO) and nicotine have opposing effects on gastric integrity. The present study examined the possible therapeutic benefit of NO in nicotine-treated rats with stress-induced gastric ulceration. METHODS: Rats drank a nicotine solution while control rats drank tap water for 20 days. The alkoloid was then replaced by water with or without supplementation of isosorbide dinitrate (NO donor) for an additional 10 days. Isosorbide dinitrate was given twice shortly before experiments (acute) or three times daily by oral gavages for 10 days after the rats stopped drinking nicotine solution. At the end of experiments, ulcer index, gastric adhesion mucus content and MPO activity were measured and analysed. RESULTS: Nicotine treatment decreased gastric mucus content and intensified stress-induced gastric ulcer. A higher ulcer index persisted even after the rats stopped drinking nicotine solution for 10 days. Acute NO donor showed no benefit on both mucus and ulcer index in nicotine treatment or/and stress condition. Chronic NO donor treatment reversed the worsening action of nicotine in stomach. Stress increased gastric mucosal myeloperoxidase (MPO) activity, which was antagonized by chronic NO treatment. However, nicotine was unlikely to change mucosal MPO activity. CONCLUSION: The intensifying action of nicotine on stress-induced gastric ulceration persists for 10 days after cessation. Nicotine treatment significantly decreases gastric mucus content that can be restored by chronic NO donor treatment. The present study suggests that NO antagonizes the ulcerogenic action of nicotine through a cytoprotective way.
机译：目的：压力在人和实验动物中诱发胃溃疡。人们在压力下倾向于抽更多的烟。一氧化氮（NO）和尼古丁对胃的完整性有相反的影响。本研究检查了NO在烟碱治疗的应激性胃溃疡大鼠中的可能的治疗益处。方法：大鼠饮用尼古丁溶液，对照组大鼠饮用自来水20天。然后将生物碱用水替换为补充或不补充硝酸异山梨酯（NO供体）的水，持续另外10天。在大鼠实验前不久（急性）给予两次硝酸异山梨酯，或者在大鼠停止饮用尼古丁溶液后连续10天每天口服3次给予硝酸异山梨酯。在实验结束时，测量并分析溃疡指数，胃粘膜粘液含量和MPO活性。结果：尼古丁治疗降低了胃粘液含量并加剧了应激性胃溃疡。即使在大鼠停止饮用尼古丁溶液10天后，较高的溃疡指数仍然存在。急性NO供体在尼古丁治疗或/和应激状态下对黏液和溃疡指数均无益处。长期的NO供体治疗逆转了尼古丁在胃中的恶化作用。压力增加了胃粘膜髓过氧化物酶（MPO）的活性，而慢性NO治疗则拮抗这一作用。但是，尼古丁不太可能改变粘膜MPO活性。结论：尼古丁在戒断后持续10天对应激性胃溃疡的强化作用持续存在。尼古丁治疗可显着降低可通过长期NO供体治疗恢复的胃粘液含量。本研究表明，NO通过细胞保护作用拮抗尼古丁的致溃疡作用。

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