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首页> 外文期刊>Digestive Diseases and Sciences >Tanshinone IIA Ameliorates Trinitrobenzene Sulfonic Acid (TNBS)-Induced Murine Colitis
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Tanshinone IIA Ameliorates Trinitrobenzene Sulfonic Acid (TNBS)-Induced Murine Colitis

机译：丹参酮IIA改善三硝基苯磺酸（TNBS）诱导的小鼠结肠炎

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Inflammatory bowel diseases are characterized by proinflammatory cytokines, oxidative stress, and tissue damage. Recently, tanshinone had been shown to act as an antioxidant, and to have anti-inflammatory bioactivity. The study was carried out to investigate the effect of tanshinone IIA on the inflammatory response of experimental colitis. Murine colitis was induced by trinitrobenzene sulfonic acid (TNBS). Ten or 20 mg tanshinone IIA was administrated to mice 4 h before the induction of colitis, and repeated daily until the mice were sacrificed. Colonic inflammation was examined by histological analysis, myeloperoxidase (MPO) activity, and the production of proinflammatory cytokines in colonic tissue. Activation of nuclear factor-kappa B was identified by western blot and immunohistochemistry, and oxidative stress was shown by glutathione (GSH) level in tissue. The mice with colitis treated by tanshinone IIA showed less tissue damage, lower MPO activity, less production of TNF-α and IL-1β, a higher level of GSH in colonic tissue, and downregulated activation of nuclear factor-kappa B in lamina propria mononuclear cells, compared with those of the untreated colitis group. Our data indicates that tanshinone IIA inhibits inflammatory response of colitis by downregulating the production of proinflammatory cytokines, and attenuating oxidative stress, which suggests that tanshinone IIA may be a new potential management for inflammatory bowel diseases.
机译：炎症性肠疾病的特征在于促炎性细胞因子，氧化应激和组织损伤。最近，丹参酮已被证明可以起到抗氧化剂的作用，并具有抗炎的生物活性。进行该研究以研究丹参酮IIA对实验性结肠炎的炎症反应的影响。三硝基苯磺酸（TNBS）诱发小鼠结肠炎。在诱发结肠炎之前4小时，向小鼠施用10或20 mg丹参酮IIA，每天重复一次，直至处死小鼠。通过组织学分析，髓过氧化物酶（MPO）活性以及结肠组织中促炎细胞因子的产生来检查结肠炎症。通过蛋白质印迹和免疫组织化学鉴定核因子-κB的活化，并通过组织中的谷胱甘肽（GSH）水平显示氧化应激。丹参酮IIA治疗的结肠炎小鼠表现出更少的组织损伤，更低的MPO活性，更少的TNF-α和IL-1β产生，结肠组织中GSH的更高水平以及固有层固有核中核因子-κB的激活下调与未治疗的结肠炎组相比。我们的数据表明，丹参酮IIA通过下调促炎细胞因子的产生并减弱氧化应激来抑制结肠炎的炎症反应，这表明丹参酮IIA可能是炎症性肠病的一种新的潜在治疗方法。

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