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目的:研究一氧化氮合酶抑制物非对称性二甲基精氨酸(ADMA)在不同因素诱发的胃黏膜损伤中的作用,并初步探讨其机制。方法:用乙醇、吲哚美辛、应激诱发大鼠胃黏膜损伤模型,检测胃黏膜溃疡指数(UI),一氧化氮(NO)和ADMA水平,以及二甲基精氨酸-二甲胺水解酶(DDAH)的活性;检测幽门螺旋杆菌(Hp)处理胃黏膜上皮细胞(GES-1)细胞培养液中NO,ADMA和TNF-α水平,以及细胞中DDAH活性。结果:乙醇、吲哚美辛、应激诱发大鼠胃黏膜损伤的同时ADMA水平显著升高以及DDAH活性下降;Hp处理GES-1细胞24 h后,ADMA和TNF-α水平显著升高,DDAH活性下降;外源性ADMA也能显著升高GES-1细胞TNF-α水平。结论:ADMA是促进胃黏膜损伤的重要因子,除抑制NO生成外,还具有直接致炎作用。
AIM: To investigate the role of asymmetric dimethylarginine (ADMA), a nitric oxide synthase inhibitor, in gastric mucosal injury induced by different factors and to explore its mechanism. Methods: Gastric mucosal injury induced by stress was induced by ethanol and indomethacin. The ulcer index (UI), nitric oxide (NO) and ADMA level in gastric mucosa were measured, and the levels of dimethylarginine-dimethylamine (DDAH). The levels of NO, ADMA and TNF-α in the culture medium of gastric epithelial cells (GES-1) treated by H. pylori and the activity of DDAH in the cells were detected. Results: Ethanol and indomethacin significantly increased ADMA level and DDAH activity in gastric mucosal injury induced by stress. The levels of ADMA and TNF-α in HES-treated GES-1 cells were significantly increased at 24 h Activity decreased; exogenous ADMA also significantly increased GES-1 cells TNF-α levels. Conclusion: ADMA is an important factor in promoting gastric mucosal injury. In addition to inhibiting NO production, ADMA also has a direct inflammatory effect.