Chow J Y, Ma L, Cho C H
Department of Pharmacology, Faculty of Medicine, The University of Hong Kong, PR China.
Eur J Pharmacol. 1998 Jan 26;342(2-3):253-60. doi: 10.1016/s0014-2999(97)01483-0.
The roles of neutrophil aggregation, inducible nitric oxide synthase activation and chemoattractant, leukotriene B4, in potentiation of the cigarette smoke effect on ethanol-induced gastric mucosal damage were studied. Smoke exposure markedly increased gastric lesion formation following ethanol administration and this was accompanied by substantial increase in gastric mucosal leukotriene B4 concentration, myeloperoxidase and inducible nitric oxide synthase activities. Antineutrophil serum or aminoguanidine pretreatment significantly attenuated both gastric mucosal lesion formation and inducible nitric oxide synthase activity. The increased myeloperoxidase activity was abolished by antineutrophil serum but not by aminoguanidine. These data indicated that both neutrophil mobilization and inducible nitric oxide synthase activation in the gastric mucosa play an important role in the potentiating action of cigarette smoke on ethanol-induced gastric mucosal lesion formation. Increased synthesis of nitric oxide from inducible nitric oxide synthase during gastric damage may be secondary to neutrophil infiltration in the gastric mucosa. Chemoattractant leukotriene B4 could also contribute to neutrophil recruitment in the tissue.
研究了中性粒细胞聚集、诱导型一氧化氮合酶激活以及趋化因子白三烯B4在增强香烟烟雾对乙醇诱导的胃黏膜损伤作用中的作用。暴露于香烟烟雾显著增加了乙醇给药后的胃损伤形成，同时胃黏膜白三烯B4浓度、髓过氧化物酶和诱导型一氧化氮合酶活性也大幅增加。抗中性粒细胞血清或氨基胍预处理显著减轻了胃黏膜损伤形成和诱导型一氧化氮合酶活性。抗中性粒细胞血清消除了增加的髓过氧化物酶活性，但氨基胍没有。这些数据表明，胃黏膜中的中性粒细胞动员和诱导型一氧化氮合酶激活在香烟烟雾对乙醇诱导的胃黏膜损伤形成的增强作用中起重要作用。胃损伤期间诱导型一氧化氮合酶产生的一氧化氮增加可能继发于胃黏膜中的中性粒细胞浸润。趋化因子白三烯B4也可能有助于组织中中性粒细胞的募集。
