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氢气介导对葡聚糖硫酸钠诱导的结肠炎症的抑制作用。

Hydrogen mediates suppression of colon inflammation induced by dextran sodium sulfate.

作者信息

Kajiya Mikihito, Silva Marcelo J B, Sato Kimihiro, Ouhara Kazuhisa, Kawai Toshihisa

机构信息

Department of Immunology, The Forsyth Institute, Boston, MA 02115, USA.

出版信息

Biochem Biophys Res Commun. 2009 Aug 14;386(1):11-5. doi: 10.1016/j.bbrc.2009.05.117. Epub 2009 May 30.

Abstract

By its antioxidant effect, molecular hydrogen gas (H2) was reported to protect organs from tissue damage induced by ischemia reperfusion. To evaluate its anti-inflammatory effects, we established a mouse model of human inflammatory bowel disease (IBD) by supplying mice with water containing (1) dextran sodium sulfate (DSS) (5%), (2) DSS (5%) and H2, or (3) H2 only ad libitum up to 7 days. At day-7, DSS-induced pathogenic outcomes including, loss of body weight, increase of colitis score, pathogenic shortening of colon length, elevated level of IL-12, TNF-alpha and IL-1beta in colon lesion, were significantly suppressed by the addition of H2 to DSS solution. Histological analysis also revealed that the DSS-mediated colonic tissue destruction accompanied by macrophage infiltration was remarkably suppressed by H2. Therefore, the present study indicated that H2 can prevent the development of DSS-induced colitis in mice.

摘要

据报道,分子氢气(H2)通过其抗氧化作用保护器官免受缺血再灌注诱导的组织损伤。为了评估其抗炎作用,我们建立了一种人类炎症性肠病(IBD)小鼠模型,方法是给小鼠随意提供含有(1)葡聚糖硫酸钠(DSS)(5%)、(2)DSS(5%)和H2或(3)仅H2的水,持续7天。在第7天,DSS诱导的致病结果,包括体重减轻、结肠炎评分增加、结肠长度病理性缩短、结肠病变中IL-12、TNF-α和IL-1β水平升高,通过在DSS溶液中添加H2得到显著抑制。组织学分析还显示,H2显著抑制了DSS介导的伴有巨噬细胞浸润的结肠组织破坏。因此,本研究表明H2可以预防小鼠DSS诱导的结肠炎的发展。

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