摘要
神经肽特别是P物质(SP)可以导致眼部炎症反应。SP是在炎症过程中从感觉神经末梢和各种免疫细胞分泌出来的一种十一氨基酸多肽。SP通过其结合的高亲和力的神经激肽-1受体(NK1R)来调节眼部炎症。这种受体在神经、免疫细胞和上皮细胞上表达。 SP是神经源性炎症的重要介质,能增加微血管通透性、使血管扩张、血浆外渗从而导致组织水肿。此外,巨噬细胞释放细胞因子、趋化因子等炎症介质并能响应SP刺激生长因子。抑制的P物质的活性能通过阻断神经肽和SP受体拮抗剂释放改善眼部炎症。它能恢复免疫特性,并提高了一些与炎症相关疾病如角膜混浊、眼穿孔和血管生成的临床终点。 本文总结了SP在眼部的炎症反应的作用,并讨论了SP药物阻断剂治疗动物模型眼部炎症以及人类普遍疾病的作用。
关键词: P物质,速激肽,神经肽,眼部炎症,神经源性炎症,角膜新生血管。
图形摘要
Current Drug Targets
Title:Substance P and its Inhibition in Ocular Inflammation
Volume: 17 Issue: 11
Author(s): Fabio Bignami, Paolo Rama, Giulio Ferrari
Affiliation:
关键词: P物质,速激肽,神经肽,眼部炎症,神经源性炎症,角膜新生血管。
摘要: Neuropeptides, and specifically Substance P (SP), can crucially contribute to the ocular inflammatory response. SP is an undecapeptide that is secreted from sensory nerve endings and from various immune cells during inflammation. SP modulates ocular inflammation through its binding with the high-affinity neurokinin-1 receptor (NK-1R). This receptor is expressed on nerves, immune cells, and epithelial cells.
SP is a key mediator of neurogenic inflammation as it induces increased microvascular permeability, vasodilatation, plasma extravasation, and subsequent tissue edema. In addition, macrophages can release inflammatory mediators such as interleukins, chemokines, and growth factors in response to SP stimulation. Inhibition of SP activity, either through blockade of the neuropeptide release or the use of SP receptor antagonists, ameliorates ocular inflammation, it restores immune privilege and improves a number of clinical endpoints associated with inflammation, such as corneal opacity, ocular perforation, and angiogenesis.
This review of the literature will summarize the role of SP in the ocular inflammatory response (with an emphasis on the ocular surface). In addition, it will review the therapeutic effects of SP blockade to control ocular inflammation (i) in animal models and (ii) in highly prevalent human diseases.
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Cite this article as:
Fabio Bignami, Paolo Rama, Giulio Ferrari , Substance P and its Inhibition in Ocular Inflammation, Current Drug Targets 2016; 17 (11) . https://dx.doi.org/10.2174/1389450116666151019100216
DOI https://dx.doi.org/10.2174/1389450116666151019100216 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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