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首页> 外文期刊>Life sciences >Mechanistic study of adverse actions of cigarette smoke exposure on acetic acid-induced gastric ulceration in rats.
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Mechanistic study of adverse actions of cigarette smoke exposure on acetic acid-induced gastric ulceration in rats.

机译：香烟烟雾暴露对乙酸诱发的大鼠胃溃疡的不良作用的机理研究。

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摘要

Cigarette smoking is associated with peptic ulceration in humans. A mechanistic study of the potentiating effects of cigarette smoking on acetic acid-induced gastric ulceration in rats was hence performed. Rats were exposed to 0, 2 or 4% of cigarette smoke for three 1-hr periods during the 24 hr starvation before ulcer induction. Cigarette smoke exposure potentiated ulcer formation which was accompanied by a reduction of gastric blood flow at the ulcer base and ulcer margin. Further studies showed that cigarette smoke exposure alone did not cause any macroscopic injury in the stomach but significantly decreased the basal gastric blood flow in a concentration-dependent manner, which was coupled with an increase in mucosal xanthine oxidase (XO) activity. Pretreatment with allopurinol (Allo, 5 mg/kg, i.v.), a XO inhibitor, partially prevented the potentiating effect of cigarette smoke exposure on ulcer formation and also significantly improved the gastric blood flow. Ulcer induction itself dramatically increased constitutive nitric oxide synthase (cNOS) activity and prostaglandin E2 (PGE2) level in the gastric mucosa. However, the increment of cNOS activity but not PGE2 level was markedly attenuated by cigarette smoke exposure. Sodium nitroprusside (SNP, 25 or 50 microg/kg, i.v.), a nitric oxide (NO) donor, completely abolished the potentiating effect of cigarette smoke exposure on ulcer formation and also reversed the adverse effect on gastric blood flow. Thus, XO activation and cNOS reduction in the gastric mucosa are closely associated with the potentiating action of cigarette smoke exposure on ulcer formation in rats.
机译：吸烟与人类消化性溃疡有关。因此，进行了吸烟对乙酸诱导的大鼠胃溃疡的增强作用的机理研究。在溃疡诱发前的24小时饥饿中，将大鼠暴露于0％，2％或4％的香烟烟雾中三个三个小时。接触香烟烟雾增强了溃疡的形成，并伴随着溃疡基部和溃疡边缘胃血流量的减少。进一步的研究表明，仅接触香烟烟雾不会对胃造成任何宏观损害，但会以浓度依赖的方式显着降低基础胃血流量，并伴有粘膜黄嘌呤氧化酶（XO）活性的增加。用XO抑制剂别嘌呤醇（Allo，5 mg / kg，i.v.）进行预处理可以部分防止香烟烟雾暴露对溃疡形成的增强作用，还可以显着改善胃血流量。溃疡诱导本身可显着增加胃粘膜中的组成型一氧化氮合酶（cNOS）活性和前列腺素E2（PGE2）水平。但是，香烟烟雾暴露会明显减弱cNOS活性的增加，但PGE2水平没有增加。一氧化氮（NO）供体硝普钠（SNP，25或50 microg / kg，i.v.）完全消除了香烟烟雾暴露对溃疡形成的增强作用，并逆转了对胃血流的不利影响。因此，胃粘膜中XO的激活和cNOS的减少与香烟暴露对大鼠溃疡形成的增强作用密切相关。

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