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牛磺酸对三硝基苯磺酸诱导的大鼠炎症性肠病的保护作用。

Protective effect of taurine on TNBS-induced inflammatory bowel disease in rats.

作者信息

Son M W, Ko J I, Doh H M, Kim W B, Park T S, Shim M J, Kim B K

机构信息

Research Laboratories, Dong-A Pharmaceutical Co., Ltd., Yongin-Shi Kyunggi-Do, Korea.

出版信息

Arch Pharm Res. 1998 Oct;21(5):531-6. doi: 10.1007/BF02975370.

Abstract

We had 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. In order to induce IBD, ethanolic TNBS was given to rats intracolonically. Then they received 500 mg/kg/day of taurine orally and were sacrificed one week after IBD induction. While ulceration and inflammation of distal colon with formation of granuloma in the vehicle-treated IBD rats two days after administration of TNBS were observed, treatment with taurine ameliorated colonic damage and decreased the incidence of diarrhea and adhesion. Also, colon weight as an index of tissue edema, which was markedly increased in the IBD rats, became significantly lower after taurine treatment. Myeloperoxidase (MPO) activity in the vehicle-treated IBD rats was substantially increased, compared with that of normal control. The taurine-treated animals significantly reduced MPO activity (35% lower) when compared with that of the vehicle-treated animals. Taurine treatment decreased both basal and formyl-methionyl leucyl phenylalanine-stimulated reactive oxygen generation from colonic tissue in the IBD rats. These results suggest that the administration of taurine reduce the inflammatory parameters in this IBD rat model by increasing defending capacity against oxidative damage.

摘要

我们之前曾报道,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减轻三硝基苯磺酸(TNBS)诱导的大鼠炎症性肠病(IBD)炎症参数的影响。为了诱导IBD,将乙醇溶解的TNBS经结肠内给予大鼠。然后它们口服500mg/kg/天的牛磺酸,并在IBD诱导后一周处死。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,而牛磺酸治疗改善了结肠损伤,降低了腹泻和粘连的发生率。此外,作为组织水肿指标的结肠重量在IBD大鼠中显著增加,在牛磺酸治疗后明显降低。与正常对照相比,赋形剂处理的IBD大鼠中的髓过氧化物酶(MPO)活性大幅增加。与赋形剂处理的动物相比,牛磺酸处理的动物显著降低了MPO活性(低35%)。牛磺酸治疗降低了IBD大鼠结肠组织基础状态下以及甲酰甲硫氨酰亮氨酰苯丙氨酸刺激下的活性氧生成。这些结果表明,给予牛磺酸可通过增强对氧化损伤的防御能力来降低该IBD大鼠模型中的炎症参数。

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