肿瘤启动子teleocidin对分离的胰岛的促胰岛素分泌作用。
Insulinotropic effect of the tumor promoter teleocidin in isolated pancreatic islets.
作者信息
Yamamoto S, Nakadate T, Fujiki H, Kato R
出版信息
Biochem Biophys Res Commun. 1983 Nov 30;117(1):78-85. doi: 10.1016/0006-291x(83)91543-7.
A tumor promoter teleocidin induced insulin secretion from isolated pancreatic islets in a concentration-dependent manner. The teleocidin-induced secretion was inhibited by p-bromophenacyl bromide, nordihydroguaiaretic acid, 3-amino-1-(3-trifluoromethylphenyl)-2-pyrazoline and 2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1,4-benzoquinone, but not by indomethacin. Insulinotropic concentrations of teleocidin stimulated 6-keto-prostaglandin F1 alpha release from pancreatic islets. These results suggest that phospholipase A2 activation and lipoxygenase product(s) are involved in the mechanism of teleocidin-induced insulin secretion.
肿瘤促进剂远藤菌素以浓度依赖的方式诱导分离的胰岛分泌胰岛素。对溴苯甲酰溴、去甲二氢愈创木酸、3-氨基-1-(3-三氟甲基苯基)-2-吡唑啉和2,3,5-三甲基-6-(12-羟基-5,10-十二碳二炔基)-1,4-苯醌可抑制远藤菌素诱导的分泌，但吲哚美辛无此作用。促胰岛素浓度的远藤菌素刺激胰岛释放6-酮-前列腺素F1α。这些结果表明，磷脂酶A2激活和脂氧合酶产物参与了远藤菌素诱导胰岛素分泌的机制。
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