Rama B N, Prasad K N
Cancer. 1986 Oct 1;58(7):1448-52. doi: 10.1002/1097-0142(19861001)58:7<1448::aid-cncr2820580712>3.0.co;2-0.
The role of adenosine 3',5'-cyclic monophosphate (cAMP) and sodium butyrate in modifying the effect of heat on murine neuroblastoma cells (NBP2) in culture was evaluated on the criterion of survival. An elevation of cellular cAMP level by prostaglandin (PG) A2, a stimulator of adenylate cyclase, and 4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (R020-1724), an inhibitor of cyclic nucleotide phosphodiesterase, only during heat treatment (43 degrees C and 40 degrees C) was sufficient to enhance the effect of heat. The extent of enhancement (additive versus synergistic) depended upon the cAMP stimulating agent and the experimental condition. When these agents were added after heat treatment for the entire observation period, they produced similar results. PGA2 and R020-1724 are known to increase the intracellular level of cAMP in these cells by three and fivefold, respectively; therefore, the effect of these agents in enhancing the heat-response may be mediated by cAMP-dependent mechanisms. The presence of sodium butyrate during heat treatment alone was ineffective; however, when it was added before or after heat treatment for the entire observation period, the survival of heated cell was markedly reduced.
以存活率为标准，评估了3',5'-环磷酸腺苷（cAMP）和丁酸钠在改变热对培养的小鼠神经母细胞瘤细胞（NBP2）作用方面的作用。仅在热处理（43℃和40℃）期间，通过前列腺素（PG）A2（一种腺苷酸环化酶刺激剂）和4-(3-丁氧基-4-甲氧基苄基)-2-咪唑啉酮（R020-1724，一种环核苷酸磷酸二酯酶抑制剂）提高细胞cAMP水平，就足以增强热效应。增强程度（相加还是协同）取决于cAMP刺激剂和实验条件。当在整个观察期的热处理后添加这些试剂时，它们产生了相似的结果。已知PGA2和R020-1724可分别使这些细胞内的cAMP水平提高三倍和五倍；因此，这些试剂增强热反应的作用可能是由cAMP依赖性机制介导的。仅在热处理期间存在丁酸钠是无效的；然而，当在整个观察期的热处理之前或之后添加时，加热细胞的存活率会显著降低。
