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应激诱导的肠道损伤的病理生理机制。

Pathophysiological mechanisms of stress-induced intestinal damage.

作者信息

Gareau Mélanie G, Silva Manuel A, Perdue Mary H

机构信息

Intestinal Disease Research Program, Department of Pathology and Molecular Medicine, McMaster University, HSC-3N5C, 1200 Main St. West, Hamilton, Ontario, L8N 3Z5, Canada.

出版信息

Curr Mol Med. 2008 Jun;8(4):274-81. doi: 10.2174/156652408784533760.

Abstract

Stress has been shown to have both central and peripheral effects, promoting psychological illness (such as anxiety and depression), as well influencing peripheral disease in the intestine. Stress in humans can exacerbate symptoms of irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD), lowering visceral pain thresholds and decreasing mucosal barrier function. Studies in rodents have revealed that both acute and chronic exposure to stressors can lead to pathophysiology of the small and large intestine, including altered ion secretion and increased epithelial permeability (by both transcellular and paracellular pathways). Prolonged exposure to stress can induce low-grade inflammation, cause ultrastructural epithelial abnormalities, and alter bacterial-host interactions allowing greater microbial translocation. In this review, we discuss the stress response and the effects of both acute and chronic stress to induce pathophysiological damage to the gut. We present the potential pathways involved, and the proposed mechanisms of action mediating the effects. Furthermore, we explore the impact of early life stress on colonic physiology in neonatal rodents and the implications for gut dysfunction in adulthood.

摘要

压力已被证明具有中枢和外周效应,既会引发心理疾病(如焦虑和抑郁),也会影响肠道的外周疾病。人类的压力会加剧肠易激综合征(IBS)和炎症性肠病(IBD)的症状,降低内脏疼痛阈值并降低黏膜屏障功能。对啮齿动物的研究表明,急性和慢性暴露于应激源都会导致小肠和大肠的病理生理学变化,包括离子分泌改变和上皮通透性增加(通过跨细胞和细胞旁途径)。长期暴露于压力会诱发低度炎症,导致上皮超微结构异常,并改变细菌与宿主的相互作用,从而使微生物更容易发生移位。在这篇综述中,我们讨论了应激反应以及急性和慢性应激对肠道诱导病理生理损伤的影响。我们介绍了其中涉及的潜在途径以及介导这些影响的作用机制。此外,我们探讨了早期生活压力对新生啮齿动物结肠生理的影响以及对成年后肠道功能障碍的影响。

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