Background
Astressin 2B is selective and potent antagonist of corticotropin-releasing factor receptor 2 (CRF2) (IC50 values are 1.3 and > 500 nM for CRF2 and CRF1 respectively) that antagonizes CRF2-mediated inhibition of gastric emptying.
Ach-mediated effects on cell adhesion are blocked by astressin 2b, a CRF2 antagonist, suggesting that Ach action depends partly on CRF2 signaling[4].
Astressin-2B also exacerbated the intestinal ulcerogenic response induced by indomethacin. Urocortin I prevented indomethacin-induced intestinal lesions, together with the suppression of bacterial invasion and an increase in mucosal MPO activity and iNOS expression. Urocortin I suppressed the hypermotility response to indomethacin, and this effect was also abrogated by astressin-2B[2]. In mcie, Central administration of Ucn1 increased significantly the number of entries into the chamber of the unknown male, without changing the time of interaction and this effect was blocked by astressin2B[1]. NmU, a potent endogenous anorectic, serves as a catabolic signaling molecule in the brain. For an investigation of the possible role of receptors in mediating hyperthermia, the animals were treated with astressin 2B, a CRH2 receptor antagonist. NmU increased the colon temperature, maximal action being observed at 2-3h[3].
参考文献:
[1]. Bagosi Z, Karasz G, et,al. The effects of CRF and urocortins on the sociability of mice. Brain Res. 2017 May 15;1663:114-122. doi: 10.1016/j.brainres.2017.03.003. Epub 2017 Mar 14. PMID: 28315311.
[2]. Kubo Y, Kumano A, et,al. Urocortin prevents indomethacin-induced small intestinal lesions in rats through activation of CRF2 receptors. Dig Dis Sci. 2010 Jun;55(6):1570-80. doi: 10.1007/s10620-009-0930-1. Epub 2009 Aug 26. PMID: 19707872.
[3]. Telegdy G, Adamik A. Mediators involved in the hyperthermic action of neuromedin U in rats. Regul Pept. 2014 Jun-Aug;192-193:24-9. doi: 10.1016/j.regpep.2014.07.004. Epub 2014 Aug 7. PMID: 25108055.
[4]. Pelissier-Rota M, Chartier NT, et,al. A crosstalk between muscarinic and CRF2 receptors regulates cellular adhesion properties of human colon cancer cells. Biochim Biophys Acta Mol Cell Res. 2017 Jul;1864(7):1246-1259. doi: 10.1016/j.bbamcr.2017.04.008. Epub 2017 Apr 18. PMID: 28432022.
Astressin 2B 是促肾上腺皮质激素释放因子受体 2 (CRF2) 的选择性强效拮抗剂（IC50 值为 1.3 和 >；CRF2 和 CRF1 分别为 500 nM），可拮抗 CRF2 介导的胃排空抑制。
Ach 介导的细胞粘附作用被 CRF2 拮抗剂 astressin 2b 阻断，表明 Ach 作用部分取决于 CRF2 信号[4]。
Astressin-2B 还加剧了吲哚美辛诱导的肠道溃疡反应。 Urocortin I 可预防吲哚美辛引起的肠道损伤，同时抑制细菌入侵并增加粘膜 MPO 活性和 iNOS 表达。 Urocortin I 抑制对吲哚美辛的过度运动反应，并且这种作用也被 astressin-2B[2] 消除。在 mcie 中，Ucn1 的中央管理显着增加了未知男性进入腔室的次数，而没有改变相互作用的时间，并且这种作用被 astressin2B[1] 阻断。 NmU 是一种有效的内源性厌食剂，在大脑中充当分解代谢信号分子。为了研究受体在介导体温过高中的可能作用，动物接受了 astressin 2B（一种 CRH2 受体拮抗剂）治疗。 NmU 增加结肠温度，在 2-3 小时观察到最大作用[3]。
Protocol
| Cell experiment [1]: |
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Cell lines
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A431 epidermoid cells
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Preparation Method
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cells were pretreated overnight with Astressin 2b (1 μM). Non-adherent cells were removed by washing three times with PBS, and cell adhesion was estimated by a colorimetric cell proliferation assay.
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Reaction Conditions
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Astressin 2b (1 μM) overnight
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Applications
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Ach-mediated effects on cell adhesion are blocked by astressin 2b, a CRF2 antagonist, suggesting that Ach action depends partly on CRF2 signaling.
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| Animal experiment [2]: |
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Animal models
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Male Sprague-Dawley rats (240-280 g)
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Preparation Method
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The animals were administered indomethacin and killed 24 h later under deep ether anesthesia. Ucn I (a CRFR1 and CRFR2 agonist: 2 20 μg/kg) or astressin (a nonselective CRFR antagonist: 50 μg/kg) was given i.v. 10 min before the administration of indomethacin. NBI-27914 or astressin 2B (60 μg/kg) was given i.v. 10 min before the administration of Ucn I or indomethacin.
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Dosage form
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60 μg/kg astressin 2B
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Applications
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Astressin 2B also exacerbated the intestinal ulcerogenic response induced by indomethacin. Urocortin I prevented indomethacin-induced intestinal lesions, together with the suppression of bacterial invasion and an increase in mucosal MPO activity and iNOS expression. Urocortin I suppressed the hypermotility response to indomethacin, and this effect was also abrogated by astressin-2B.
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参考文献:
[1]. Pelissier-Rota M, Chartier NT,et,al. A crosstalk between muscarinic and CRF2 receptors regulates cellular adhesion properties of human colon cancer cells. Biochim Biophys Acta Mol Cell Res. 2017 Jul;1864(7):1246-1259. doi: 10.1016/j.bbamcr.2017.04.008. Epub 2017 Apr 18. PMID: 28432022.
[2]. Kubo Y, Kumano A, et,al. Urocortin prevents indomethacin-induced small intestinal lesions in rats through activation of CRF2 receptors. Dig Dis Sci. 2010 Jun;55(6):1570-80. doi: 10.1007/s10620-009-0930-1. Epub 2009 Aug 26. PMID: 19707872.
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