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Role of metabolic changes of mucosal layer in the intestinal barrier dysfunction following trauma/hemorrhagic shock

机译:粘膜层代谢变化在创伤/出血休克后肠道屏障功能障碍中的作用

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BackgroundThe mucosal layer plays an important role in regulating the intestinal barrier function. However, the underlying mechanisms of intestinal barrier dysfunction caused by trauma-hemorrhagic shock (THS) are still unknown. MethodsIn this study, we examined the barrier damages, inflammatory responses as well as the metabolic changes of the mucosal layer of the colon in a THS rat model. ResultsThe results showed that compared to the rats treated with trauma only, THS induced marked failure of intestinal barrier characterized by increased intestinal permeability, inflammatory cell infiltration and decreased expression of genes involved in epithelial integrity. Moreover, decreased colonic mucus content and goblet cell numbers indicated that the mucosal layer was also impaired in response to THS. This was companied by the anomalous inflammatory responses in the tissue. Finally, microdialysis catheter examination showed that metabolites including glycerol, glucose, lactate and pyruvate, glutamate and glutamine were also altered by THS. ConclusionOur results provide evidence that mucus layer-associated metabolic changes may contribute to the THS-induced intestinal barrier dysfunction.
机译:背景技术粘膜层在调节肠道屏障功能方面发挥着重要作用。然而,创伤引起的肠道障碍功能障碍的潜在机制仍然未知。方法这项研究,我们检查了屏障损伤,炎症反应以及在THS大鼠模型中结肠粘膜层的代谢变化。结果表明,与肠道屏障的肠道势诱导的大鼠相比,其特征在于肠道势,炎症细胞浸润和上皮完整性的基因的表达减少,诱导肠道屏障的标记失效。此外,降低的结肠粘液含量和脚卵细胞数表明粘膜层响应于THS也受到损害。这是由组织中的异常炎症反应伴随。最后,MicrodiaLysis导管检查表明,由甘油,葡萄糖,乳酸和丙酮酸,谷氨酸和谷氨酰胺的代谢物也被改变。结论Rour结果提供了证据表明粘液相关的代谢变化可能有助于诱导的肠道屏障功能障碍。

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