Son M, Ko J I, Kim W B, Kang H K, Kim B K
Research Laboratories of Dong-A Pharmaceutical Co., Ltd, Yongin-shi, Kyunggi-do, Korea.
Adv Exp Med Biol. 1998;442:291-8. doi: 10.1007/978-1-4899-0117-0_37.
We previously reported that the protective effect of taurine against indomethacin-induced gastric mucosal injury was due to its antioxidant effects which inhibited lipid peroxidation and neutrophil activation. In this study, we examined the effect of taurine on reducing the inflammatory parameters of trinitrobenzene sulfonic acid (TNBS)-induced inflammatory bowel disease (IBD) in rats. To induce IBD, rats were given ethanolic TNBS intracolonically. The rats then received 500 mg/kg/day of taurine per orally. The rats were sacrificed one week after IBD induction. Ulceration and inflammation of the distal colon with formation of granuloma in the vehicle-treated IBD rats after two days of administration of TNBS were observed. Treatment with 0.5 g/kg of taurine by the oral route ameliorated colonic damage and decreased the incidence of diarrhea and adhesions. Colon weight (an index of tissue edema) was markedly increased in the IBD rats after administration of TNBS, but was significantly lower after taurine treatment. Myeloperoxidase (MPO) activity in the vehicle-treated IBD rats was substantially increased compared with that of the control. The taurine-treated animals showed reduced MPO activity (35% lower) when compared with that of the vehicle-treated animals. Taurine treatment decreased basal and formyl-methionyl leucyl phenylalanine (FMLP) stimulated reactive oxygen generation in colonic tissue of the IBD rat compared with vehicle treatment after one week. These results suggest that administration of taurine reduced the inflammatory parameters in this rat model of IBD by increasing the defenses against oxidative insult.
我们之前报道过,牛磺酸对吲哚美辛诱导的胃黏膜损伤的保护作用归因于其抗氧化作用,该作用抑制了脂质过氧化和中性粒细胞活化。在本研究中,我们检测了牛磺酸对降低三硝基苯磺酸(TNBS)诱导的大鼠炎症性肠病(IBD)炎症参数的作用。为诱导IBD,给大鼠结肠内注射乙醇溶液中的TNBS。然后大鼠口服500mg/kg/天的牛磺酸。IBD诱导一周后处死大鼠。在给予TNBS两天后,观察到在赋形剂处理的IBD大鼠中,远端结肠出现溃疡和炎症,并形成肉芽肿。口服0.5g/kg牛磺酸治疗可改善结肠损伤,并降低腹泻和粘连的发生率。TNBS给药后,IBD大鼠的结肠重量(组织水肿指标)显著增加,但牛磺酸治疗后明显降低。与对照组相比,赋形剂处理的IBD大鼠的髓过氧化物酶(MPO)活性大幅增加。与赋形剂处理的动物相比,牛磺酸处理的动物的MPO活性降低(低35%)。与赋形剂处理相比,牛磺酸治疗一周后降低了IBD大鼠结肠组织中基础和甲酰甲硫氨酰亮氨酰苯丙氨酸(FMLP)刺激的活性氧生成。这些结果表明,牛磺酸给药通过增强对氧化损伤的防御作用降低了该IBD大鼠模型中的炎症参数。