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Crit Care Med. 2006 Apr;34(4):1119-25. doi: 10.1097/01.CCM.0000206467.19509.C6.
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A2a receptors mediate inhibitory effects of adenosine on colonic motility in the presence of experimental colitis.在实验性结肠炎存在的情况下，A2a受体介导腺苷对结肠动力的抑制作用。
Inflamm Bowel Dis. 2006 Feb;12(2):117-22. doi: 10.1097/01.MIB.0000198535.13822.a9.
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Effect of adenosine A2A receptor activation in murine models of respiratory disorders.腺苷A2A受体激活在小鼠呼吸系统疾病模型中的作用。
Am J Physiol Lung Cell Mol Physiol. 2006 May;290(5):L1036-43. doi: 10.1152/ajplung.00422.2005. Epub 2005 Dec 9.
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Adenosine augments IL-10 production by macrophages through an A2B receptor-mediated posttranscriptional mechanism.腺苷通过A2B受体介导的转录后机制增强巨噬细胞产生白细胞介素-10。
J Immunol. 2005 Dec 15;175(12):8260-70. doi: 10.4049/jimmunol.175.12.8260.
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Adenosine inhibits the release of interleukin-1beta in activated human peripheral mononuclear cells.腺苷可抑制活化的人外周血单个核细胞中白细胞介素-1β的释放。
Cytokine. 2005 Aug 21;31(4):258-63. doi: 10.1016/j.cyto.2005.05.002.
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Activation of A2A adenosine receptor attenuates intestinal inflammation in animal models of inflammatory bowel disease.A2A 腺苷受体的激活可减轻炎症性肠病动物模型中的肠道炎症。
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Adenosine: an endogenous regulator of innate immunity.腺苷：一种先天性免疫的内源性调节因子。
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Adenosine stimulates CREB activation in macrophages via a p38 MAPK-mediated mechanism.腺苷通过p38丝裂原活化蛋白激酶介导的机制刺激巨噬细胞中的CREB激活。
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腺苷A2A受体激动剂CGS 21680不能改善葡聚糖硫酸钠诱导的小鼠结肠炎病程。

The adenosine A2A receptor agonist CGS 21680 fails to ameliorate the course of dextran sulphate-induced colitis in mice.

作者信息

Selmeczy Z, Csóka B, Pacher P, Vizi E S, Haskó G

机构信息

Department of Pharmacology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.

出版信息

Inflamm Res. 2007 May;56(5):204-9. doi: 10.1007/s00011-006-6150-7.

DOI:10.1007/s00011-006-6150-7
PMID:17588136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2225471/
Abstract

OBJECTIVE

In this study we investigated the effect of CGS 21680 (2-p-(2-Carboxyethyl)phenethylamino-5-N-ethylcarboxamidoadenosine hydrochloride), an adenosine A2A receptor agonist, in a model of dextran sulphate sodium (DSS)-induced colitis.

METHODS

NMRI mice were fed 5 % (w/v) DSS, and were treated intraperitoneally with 0.5 mg/kg CGS 21680 or vehicle for 10 days. Changes of bodyweight, colon length, the incidence of rectal bleeding, levels of macrophage inflammatory protein (MIP)-1alpha, MIP-2, interferon gamma, interleukin (IL)-1beta, IL-12 and tumour necrosis factor-alpha from homogenates of colon biopsies, and the release of [3H]acetylcholine (ACh) from longitudinal muscle strip were determined.

RESULTS

DSS significantly decreased bodyweight, colon length, and it increased the incidence of rectal bleeding and levels of MIP-1alpha, MIP-2 and IL-1beta compared to DSS-untreated animals. CGS 21680 had no effect on these changes. No change could be observed in release of ACh in DSS-induced colitis with or without CGS 21680.

CONCLUSION

In summary, CGS 21680 is ineffective in ameliorating DSS-induced colitis in mice.

摘要

目的

在本研究中，我们调查了腺苷A2A受体激动剂CGS 21680（2 - 对 -（2 - 羧乙基）苯乙氨基 - 5 - N - 乙基甲酰胺基腺苷盐酸盐）在葡聚糖硫酸钠（DSS）诱导的结肠炎模型中的作用。

方法

给NMRI小鼠喂食5%（w/v）的DSS，并腹腔注射0.5 mg/kg的CGS 21680或赋形剂，持续10天。测定体重变化、结肠长度、直肠出血发生率、结肠活检匀浆中巨噬细胞炎性蛋白（MIP）-1α、MIP - 2、干扰素γ、白细胞介素（IL）-1β、IL - 12和肿瘤坏死因子 - α的水平，以及纵向肌条中[3H]乙酰胆碱（ACh）的释放。

结果

与未用DSS处理的动物相比，DSS显著降低了体重和结肠长度，并增加了直肠出血发生率以及MIP - 1α、MIP - 2和IL - 1β的水平。CGS 21680对这些变化没有影响。在有或没有CGS 21680的DSS诱导的结肠炎中，未观察到ACh释放的变化。

结论

总之，CGS 21680在改善小鼠DSS诱导的结肠炎方面无效。