The effect of restraint stress on the normal colon and on intestinal inflammation in a model of experimental colitis
The effect of restraint stress on the normal colon and on intestinal inflammation in a model of experimental colitis
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DOI：
10.1007/s10620-007-9827-z
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发表时间：
2008-01-01
影响因子：
3.1
通讯作者：
Goldin, Eran
中科院分区：
文献类型：
--
作者：
Israeli, Eran;Hershcovici, Tiberiu;Goldin, Eran
在结肠炎动物模型中，应激可诱导炎症的发展。研究了束缚应激对正常结肠粘膜氧化损伤和抗氧化剂的影响。在TNBS-结肠炎模型中研究了应激对炎症指标严重程度的影响，以及粘膜P物质（SP）作为这种影响的介质的重要性。束缚应激显著增加了正常结肠中的丙二醛水平，降低了低分子量抗氧化剂的水平。ATP和粘膜的“能荷”大幅下降，慢性应激。慢性应激使2，4，6-三硝基苯磺酸（TNBS）诱导的结肠炎的炎症程度恶化。粘蛋白SP含量不受慢性应激的影响，但诱导结肠炎后增加。当暴露于压力后诱发结肠炎时，这种增加更大。我们的结论是，慢性束缚应激导致氧化损伤的正常结肠和加重肠道炎症诱导的TNBS。这种作用可能是由SP介导的。
Stress may induce development of inflammation in animal models of colitis. The effects of restraint stress on oxidative damage and on antioxidants in the normal colonic mucosa were studied. The effect of stress on the severity of indicators of inflammation, as well as the importance of mucosal substance P (SP) as a mediator of this effect were investigated in the TNBS-colitis model. Restraint stress significantly increased malondialdehyde levels and reduced levels of low-molecular-weight-antioxidants in the normal colon. ATP and the mucosal "energy charge" decreased substantially with chronic stress. Chronic stress worsened the extent of inflammation in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Mucosal SP content was not affected by exposure to chronic stress but increased after induction of colitis. The increase was greater when colitis was induced after exposure to stress. We conclude that chronic restraint stress causes oxidative damage to the normal colon and aggravates intestinal inflammation induced by TNBS. This effect may be mediated by SP.