Enhanced synthesis and diminished degradation of hydrogen sulfide in experimental colitis: a site-specific, pro-resolution mechanism.
Enhanced synthesis and diminished degradation of hydrogen sulfide in experimental colitis: a site-specific, pro-resolution mechanism.
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DOI：
10.1371/journal.pone.0071962
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Wallace JL
中科院分区：
文献类型：
--
作者：
Flannigan KL;Ferraz JG;Wang R;Wallace JL
硫化氢（H₂S）在整个胃肠道中产生，它有助于维持黏膜完整性、消除炎症以及修复受损组织。在发炎和受损的结肠组织中，H₂S的合成增加，但这种合成的酶源尚未完全清楚。在本研究中，测定了三种酶途径对结肠H₂S合成的作用，所采用的组织来自健康大鼠和结肠炎大鼠。还测定了结肠组织使H₂S失活的能力。来自半抗原诱导的结肠炎大鼠的结肠组织产生的H₂S明显多于健康对照组的组织。H₂S合成的最大来源是涉及半胱氨酸氨基转移酶和3 - 巯基丙酮酸硫转移酶的途径（一种α - 酮戊二酸依赖途径）。H₂S合成增加特别发生在黏膜溃疡部位，且与粒细胞浸润组织的程度无关。结肠组织使H₂S失活迅速，在黏膜溃疡部位失活明显减少。这与这些区域硫化物醌还原酶表达的显著降低相关。总之，在黏膜溃疡部位H₂S产生增加和失活减少将导致这些部位H₂S水平升高，这促进了炎症的消除和受损组织的修复。
Hydrogen sulfide (H2S) is produced throughout the gastrointestinal tract, and it contributes to maintenance of mucosal integrity, resolution of inflammation, and repair of damaged tissue. H2S synthesis is elevated in inflamed and damaged colonic tissue, but the enzymatic sources of that synthesis are not completely understood. In the present study, the contributions of three enzymatic pathways to colonic H2S synthesis were determined, with tissues taken from healthy rats and rats with colitis. The ability of the colonic tissue to inactivate H2S was also determined. Colonic tissue from rats with hapten-induced colitis produced significantly more H2S than tissue from healthy controls. The largest source of the H2S synthesis was the pathway involving cysteine amino transferase and 3-mercaptopyruvate sulfurtransferase (an α-ketoglutarate-dependent pathway). Elevated H2S synthesis occurred specifically at sites of mucosal ulceration, and was not related to the extent of granulocyte infiltration into the tissue. Inactivation of H2S by colonic tissue occurred rapidly, and was significantly reduced at sites of mucosal ulceration. This correlated with a marked decrease in the expression of sulfide quinone reductase in these regions. Together, the increased production and decreased inactivation of H2S at sites of mucosal ulceration would result in higher H2S levels at these sites, which promotes of resolution of inflammation and repair of damaged tissue.
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影响因子：
7.4
作者：
Li, Ling;Salto-Tellez, Manuel;Moore, Philip K.
通讯作者：
Moore, Philip K.
影响因子：
4.3
作者：
Lagoutte, Emilie;Mimoun, Sabria;Bouillaud, Frederic
通讯作者：
Bouillaud, Frederic
DOI：
10.1073/pnas.0705891104
发表时间：
2007-09-25
影响因子：
11.1
作者：
Elrod, John W.;Calvert, John W.;Lefer, David J.
通讯作者：
Lefer, David J.
影响因子：
6.3
作者：
Ise, F.;Takasuka, H.;Takeuchi, K.
通讯作者：
Takeuchi, K.
影响因子：
7.3
作者：
Linden, D. R.;Furne, J.;Szurszewski, J. H.
通讯作者：
Szurszewski, J. H.