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Pathways Involved in Mild Gastrointestinal Inflammation Induced by a Low Level Exposure to a Food Contaminant

机译:低水平暴露于食物污染物引起的轻度胃肠道炎症涉及的途径

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Chronic gut inflammation is associated with radical oxygen species (ROS) genesis. ROS may activate certain transcription factors such as nuclear factor κ beta (NF-κB), which regulates cyclooxygenase-2 (COX-2). Diquat, a food contaminant, is responsible for oxidative stress. This work aimed to establish the involvement of ROS and prostanoids on diquat-induced gastrointestinal inflammation and mast cell hyperplasia. Diquat increased gastrointestinal MPO activity and mast cell number. Its effect on gastric MPO activity was reversed by PD 138,387 (a COX-2 selective inhibitor) and PDTC (an inhibitor of NF-κB activation) but not by DMSO (a hydroxyl radical scavenger) and allopurinol (a xanthine oxidase inhibitor). In contrast, increased jejunal MPO activity was blocked by both DMSO, PD 138,387, and PDTC, while allopurinol enhanced it. PD 138,387 and PDTC reduced gastrointestinal mast cell number while DMSO and allopurinol did not Diquat-induced inflammation involves a gastrointestinal NF-κB activation and COX-2 dependent proinflammatory prostanoid synthesis. Furthermore, the hydroxyl radical is involved in intestinal but not gastric inflammation.
机译:慢性肠道炎症与自由基氧(ROS)的发生有关。 ROS可能激活某些转录因子,例如调节环加氧酶2(COX-2)的核因子κβ(NF-κB)。食品污染物敌草快是造成氧化应激的原因。这项工作旨在确定ROS和前列腺素类药物参与敌草快引起的胃肠道炎症和肥大细胞增生。敌草快增加了胃肠道MPO活性和肥大细胞数量。 PD 138,387(一种COX-2选择性抑制剂)和PDTC(一种NF-κB活化抑制剂)可以逆转其对胃MPO活性的影响,而DMSO(一种羟基自由基清除剂)和别嘌呤醇(一种黄嘌呤氧化酶抑制剂)可以逆转其对胃MPO活性的影响。相反,DMSO,PD 138,387和PDTC均阻止了空肠MPO活性的增加,而别嘌呤醇却增强了空肠MPO的活性。 PD 138,387和PDTC减少了胃肠道肥大细胞的数量,而DMSO和别嘌呤醇则没有。Diquat诱导的炎症涉及胃肠道NF-κB活化和COX-2依赖性前列腺炎性前列腺素的合成。此外,羟自由基与肠道炎症有关,但与胃部炎症无关。

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