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首页> 外文期刊>Digestive Diseases and Sciences >Endogenous hydrogen sulfide is an anti-inflammatory molecule in dextran sodium sulfate-induced colitis in mice.
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Endogenous hydrogen sulfide is an anti-inflammatory molecule in dextran sodium sulfate-induced colitis in mice.

机译：内源性硫化氢是葡聚糖硫酸钠诱导的小鼠结肠炎的一种抗炎分子。

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BACKGROUND: Endogenous hydrogen sulfide (H(2)S) is increasingly being recognized as an important gaseous physiological mediator. Accumulating evidence shows the functions of H(2)S in various models of disease, but rarely in colitis. In this study, we investigated the role of endogenous H(2)S in a dextran sodium sulfate (DSS)-induced colitis model. METHODS: Acute colitis was induced using 8% DSS in male BALB/c mice. The mRNA expression of cystathionine gamma-lyase (CSE), the primary synthetase of H(2)S in the gastrointestinal tract, and cystathionine-beta-synthetase (CBS) was measured by real-time RT-PCR. The amount of H(2)S in the colonic mucosa was measured by gas chromatography. Colitis severity was evaluated clinically, histologically, and biochemically under the condition of co-treatment with DL-propargylglycine (PAG), an irreversible CSE inhibitor, and sodium sulfide (Na(2)S), an H(2)S donor. RESULTS: The mRNA expression levels of CSE and CBS, and the H(2)S content in the colonic mucosa were increased with time after DSS administration. The disease activity index, which was determined by weight loss, stool consistency, and intestinal bleeding, increased after DSS administration. PAG significantly enhanced the increase in the disease activity index scores. PAG also significantly increased tissue-associated myeloperoxidase activity and thiobarbituric acid-reactive substances in the inflamed mucosa. Moreover, Na(2)S counteracted these effects of PAG. CONCLUSIONS: Taken together, the results indicated that the inhibition of endogenous H(2)S generation caused the deterioration of DSS-induced colitis. We conclude that physiological H(2)S might act as an anti-inflammatory molecule in colitis.
机译：背景：内源性硫化氢（H（2）S）越来越被认为是重要的气态生理介质。越来越多的证据显示H（2）S在各种疾病模型中的功能，但在结肠炎中却很少。在这项研究中，我们调查了内源性H（2）S在葡聚糖硫酸钠（DSS）诱导的结肠炎模型中的作用。方法：采用8％DSS诱导雄性BALB / c小鼠急性结肠炎。通过实时逆转录-聚合酶链反应（RT-PCR）测量了胱硫醚γ-裂解酶（CSE），H（2）S在胃肠道中的主要合成酶和胱硫醚β-合成酶（CBS）的mRNA表达。通过气相色谱法测量结肠粘膜中H（2）S的量。在与DL-炔丙基甘氨酸（PAG），不可逆的CSE抑制剂和硫化钠（Na（2）S），H（2）S供体共同治疗的条件下，对结肠炎的严重程度进行了临床，组织和生化评估。结果：DSS给药后，结肠黏膜中CSE和CBS的mRNA表达水平以及H（2）S含量均随时间增加。通过减重，粪便稠度和肠道出血确定的疾病活动指数在给予DSS后增加。 PAG显着增强了疾病活动指数评分的增加。 PAG还可以显着增加发炎的粘膜中与组织相关的髓过氧化物酶活性和硫代巴比妥酸反应性物质。此外，Na（2）S抵消了PAG的这些作用。结论：综上所述，结果表明内源性H（2）S生成的抑制导致DSS诱导的结肠炎的恶化。我们得出结论，生理性H（2）S可能在结肠炎中起抗炎分子的作用。

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