增加细胞环磷酸腺苷的药物可抑制增殖活性，并降低从动脉粥样硬化的人类主动脉培养的细胞中的脂质含量。
Agents that increase cellular cyclic AMP inhibit proliferative activity and decrease lipid content in cells cultured from atherosclerotic human aorta.
作者信息
Tertov V V, Orekhov A N, Smirnov V N
出版信息
Artery. 1986;13(6):365-72.
PMID:2430551
Abstract
Cholera toxin, methylisobutylxanthine and prostacyclin (PGI2) analogues as well as dibutyryl cyclic AMP inhibit by 2-7-fold 3H-thymidine uptake into intimal cells isolated from atherosclerotic human aorta in primary culture. These agents also decrease cholesteryl ester and triglyceride levels and do not affect content of phospholipids and free cholesterol in cells cultured from atherosclerotic lesions.
摘要
霍乱毒素、甲基异丁基黄嘌呤和前列环素（PGI2）类似物以及二丁酰环磷酸腺苷可使原代培养的取自动脉粥样硬化人主动脉的内膜细胞对3H-胸腺嘧啶核苷的摄取减少2至7倍。这些药物还可降低胆固醇酯和甘油三酯水平，且不影响动脉粥样硬化病变培养细胞中磷脂和游离胆固醇的含量。
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