作者: Xin Guo , Wei P. Wang , Joshua K.S. Ko , Chi H. Cho
DOI: 10.1016/S0016-5085(99)70347-1
关键词: Nitric oxide synthase 、 Leukotriene B4 、 Myeloperoxidase 、 Enema 、 Ulcerative colitis 、 Inflammatory bowel disease 、 Pharmacology 、 Immunology 、 Cyclosporin a 、 Superoxide dismutase 、 Medicine
摘要: Abstract Background & Aims: Cigarette smoking is associated with inflammatory bowel diseases (IBDs), particularly Crohn's disease, in humans. The aim of this study was to examine whether passive cigarette aggravates experimental IBD rats and clarify the underlying mechanisms. Methods: Rats were exposed smoke (CS) for 1 hour once daily 4 days before induction by 2,4,6-trinitrobenzene sulfonic acid (TNBS)-ethanol enema then killed at 2, 6, or 24 hours later. Results: Preexposure CS significantly potentiated colonic damage induced TNBS. TNBS-ethanol caused a pronounced increase myeloperoxidase activity, leukotriene B level, also inducible nitric oxide synthase its protein, messenger RNA expression. These parameters all increased further exposure CS. In contrast, superoxide dismutase activity after attenuated exposure. potentiating effects on TNBS-induced alleviated pretreatment cyclosporin A (an immunosuppressant), N G -nitro-L-arginine methylester (a inhibitor), dimethyl sulfoxide hydroxyl radical scavenger). Conclusions: results show that promotion neutrophil infiltration free production contributed effect IBD. GASTROENTEROLOGY 1999;117:884-892