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生长抑素可能参与糖皮质激素的抗炎作用。

Somatostatin may participate in the antiinflammatory actions of glucocorticoids.

作者信息

Karalis K, Mastorakos G, Sano H, Wilder R L, Chrousos G P

机构信息

Developmental Endocrinology Branch, National Institutes of Child Health and Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.

出版信息

Endocrinology. 1995 Sep;136(9):4133-8. doi: 10.1210/endo.136.9.7544277.

DOI:10.1210/endo.136.9.7544277
PMID:7544277
Abstract

Glucocorticoids are potent antiinflammatory agents. They inhibit leukocyte chemotaxis and vascular permeability and generally suppress the expression of many inflammatory mediators. Recent reports suggested that somatostatin (Sms) had significant immunomodulatory properties in vitro and in vivo. In this study we examined the effects of glucocorticoids on immunoreactive somatostatin expression in aseptic inflammatory sites of Sprague-Dawley rats given carrageenin sc. The progress of the inflammatory reaction was studied over a 7-h period with respect to the volume and cellularity of the exudate and the levels of the inflammatory mediators expressed in the inflammatory site, including immunoreactive substance P (sP), corticotropin-releasing hormone (CRH), and tumor necrosis factor-alpha (TNF alpha). Dexamethasone significantly reduced the volume and cellularity of the inflammatory exudates; in parallel, the levels of immunoreactive sP, CRH, and TNF alpha were significantly suppressed by this glucocorticoid. In contrast, immunoreactive Sms was stimulated by dexamethasone in a time-dependent fashion. These findings suggest another mechanism for suppression of the inflammatory reaction by glucocorticoids via stimulation of local Sms expression, which occurs in parallel to the inhibition of the local inflammatory mediators sP, CRH, and TNF alpha.

摘要

糖皮质激素是强效抗炎剂。它们抑制白细胞趋化性和血管通透性,并普遍抑制多种炎症介质的表达。最近的报告表明,生长抑素(Sms)在体外和体内都具有显著的免疫调节特性。在本研究中,我们检测了糖皮质激素对皮下注射角叉菜胶的Sprague-Dawley大鼠无菌炎症部位免疫反应性生长抑素表达的影响。在7小时内研究了炎症反应的进展,涉及渗出液的体积和细胞数量以及炎症部位表达的炎症介质水平,包括免疫反应性P物质(sP)、促肾上腺皮质激素释放激素(CRH)和肿瘤坏死因子-α(TNFα)。地塞米松显著降低了炎症渗出液的体积和细胞数量;同时,这种糖皮质激素显著抑制了免疫反应性sP、CRH和TNFα的水平。相反,地塞米松以时间依赖性方式刺激免疫反应性Sms。这些发现提示糖皮质激素通过刺激局部Sms表达来抑制炎症反应的另一种机制,这与抑制局部炎症介质sP、CRH和TNFα同时发生。

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