Hamilton J A
Cancer Res. 1980 Jul;40(7):2273-80.
A series of phorbol esters stimulates prostaglandin E production from both resident and starch-induced mouse peritoneal macrophages. The relative potencies of these compounds parallel their abilities both to elevate macrophage plasminogen activator levels and to function as tumor promoters in a mouse skin carcinogenesis model. Low concentrations of antiinflammatory glucocorticoids, such as dexamethasone, inhibit the enhanced prostaglandin E synthesis as a result of 12-O-tetradecanoylphorbol-13-acetate action. The same glucocorticoids also inhibit the enhanced plasminogen activator production. On the basis of these observations, it is suggested that there might be a relationship between macrophage phospholipase activation and plasminogen activator synthesis. It is also suggested that these data might be providing insight into how 12-O-tetradecanoylphorbol-13-acetate and certain structural analogs elicit an inflammatory response and behave as tumor promoters in mouse skin.
一系列佛波酯可刺激驻留型和淀粉诱导型小鼠腹腔巨噬细胞产生前列腺素E。这些化合物的相对效力与其在小鼠皮肤致癌模型中提高巨噬细胞纤溶酶原激活剂水平以及作为肿瘤促进剂发挥作用的能力相当。低浓度的抗炎糖皮质激素，如地塞米松，可抑制因12-O-十四酰佛波醇-13-乙酸酯作用而增强的前列腺素E合成。同样的糖皮质激素也抑制增强的纤溶酶原激活剂产生。基于这些观察结果，有人提出巨噬细胞磷脂酶激活与纤溶酶原激活剂合成之间可能存在关联。还有人提出，这些数据可能有助于深入了解12-O-十四酰佛波醇-13-乙酸酯及某些结构类似物如何在小鼠皮肤中引发炎症反应并表现为肿瘤促进剂。
