| 包装: | 500μg |
| 市场价: | 5870元 |
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.
Cell lines | A431 epidermoid cells |
Preparation Method | 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. |
Reaction Conditions | Astressin 2b (1 µM) overnight |
Applications | Ach-mediated effects on cell adhesion are blocked by astressin 2b, a CRF2 antagonist, suggesting that Ach action depends partly on CRF2 signaling. |
Animal models | Male Sprague-Dawley rats (240-280 g) |
Preparation Method | 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. |
Dosage form | 60 µg/kg astressin 2B |
Applications | 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. |
| 产品描述 | 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]. References: |
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