Adcock J E, Hernandez D E, Nemeroff C B, Prange A J
Life Sci. 1983 Jun 20;32(25):2905-10. doi: 10.1016/0024-3205(83)90327-2.
Sodium salicylate (SA) has been reported to inhibit the formation of gastric ulcerations induced by aspirin, indomethacin, and absolute ethanol. In this study, SA dose-dependently inhibited gastric ulcers induced by three hours of cold-restraint stress (CRS); SA-induced cytoprotection was prevented by both acetylsalicylic acid (aspirin) and indomethacin pretreatment. Neurotensin (NT), which has previously been demonstrated to prevent the development of CRS-induced gastric ulcerations after intracisternal administration, was found to be ineffective in animals pre-treated with aspirin, and with indomethacin, as previously described. These data suggest that in the CRS model both NT- and SA-induced gastric cytoprotection require a functionally intact gastrointestinal prostaglandin synthetic pathway.
据报道，水杨酸钠（SA）可抑制由阿司匹林、吲哚美辛和无水乙醇诱导的胃溃疡形成。在本研究中，SA剂量依赖性地抑制了三小时冷束缚应激（CRS）诱导的胃溃疡；乙酰水杨酸（阿司匹林）和吲哚美辛预处理均能阻止SA诱导的细胞保护作用。之前已证明，脑池内注射神经降压素（NT）可预防CRS诱导的胃溃疡形成，但如前所述，在预先用阿司匹林和吲哚美辛处理的动物中，NT无效。这些数据表明，在CRS模型中，NT和SA诱导的胃细胞保护作用均需要功能完整的胃肠道前列腺素合成途径。
