Takagi Tomohisa, Naito Yuji, Uchiyama Kazuhiko, Okuda Toshimitsu, Suzuki Takahiro, Tsuboi Hisato, Mizushima Katsura, Handa Osamu, Yagi Nobuaki, Ichikawa Hiroshi, Yoshikawa Toshikazu
Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
Med Gas Res. 2012 Sep 3;2(1):23. doi: 10.1186/2045-9912-2-23.
The pathogenesis of inflammatory bowel disease (IBD) is complex, and an effective therapeutic strategy has yet to be established. Recently, carbon monoxide (CO) has been reported to be capable of reducing inflammation by multiple mechanisms. In this study, we evaluated the role of colonic CO insufflation in acute colitis induced by trinitrobenzene sulfonic acid (TNBS) in rats.
Acute colitis was induced with TNBS in male Wistar rats. Following TNBS administration, the animals were treated daily with 200 ppm of intrarectal CO gas. The distal colon was removed to evaluate various parameters of inflammation, including thiobarbituric acid (TBA)-reactive substances, tissue-associated myeloperoxidase (MPO) activity, and the expression of cytokine-induced neutrophil chemoattractant (CINC)-1 in colonic mucosa 7 days after TNBS administration.
The administration of TNBS induced ulceration with surrounding edematous swelling in the colon. In rats treated with CO gas, the colonic ulcer area was smaller than that of air-treated rats 7 days after TNBS administration. The wet colon weight was significantly increased in the TNBS-induced colitis group, which was markedly abrogated by colonic insufflation with CO gas. The increase of MPO activity, TBA-reactive substances, and CINC-1 expression in colonic mucosa were also significantly inhibited by colonic insufflation with CO gas.
Colonic insufflation with CO gas significantly ameliorated TNBS-induced colitis in rats. Clinical application of CO gas to improve colonic inflammatory conditions such as IBD might be useful.
炎症性肠病（IBD）的发病机制复杂，尚未确立有效的治疗策略。最近，有报道称一氧化碳（CO）能够通过多种机制减轻炎症。在本研究中，我们评估了结肠内注入CO对三硝基苯磺酸（TNBS）诱导的大鼠急性结肠炎的作用。
用TNBS诱导雄性Wistar大鼠发生急性结肠炎。给予TNBS后，动物每天接受200 ppm的直肠内CO气体治疗。在给予TNBS 7天后，切除远端结肠以评估各种炎症参数，包括硫代巴比妥酸（TBA）反应性物质、组织相关髓过氧化物酶（MPO）活性以及结肠黏膜中细胞因子诱导的中性粒细胞趋化因子（CINC）-1的表达。
给予TNBS后，结肠出现溃疡并伴有周围水肿性肿胀。在接受CO气体治疗的大鼠中，TNBS给药7天后结肠溃疡面积小于接受空气治疗的大鼠。TNBS诱导的结肠炎组结肠湿重显著增加，而结肠内注入CO气体可明显减轻这种增加。结肠内注入CO气体也显著抑制了结肠黏膜中MPO活性、TBA反应性物质和CINC-1表达的增加。
结肠内注入CO气体可显著改善TNBS诱导的大鼠结肠炎。将CO气体应用于临床以改善诸如IBD等结肠炎症状况可能是有益的。
