Leung K H, Ip M M
Int J Immunopharmacol. 1985;7(6):857-63. doi: 10.1016/0192-0561(85)90048-7.
Rat splenic natural killer (NK) cell activity against 51Cr-labeled YAC-1 or TMT-081 tumor cells can be augmented by culturing at 37 degrees C for 18 h. The protein synthesis inhibitors, cycloheximide and emetine, inhibited such NK activation and also inhibited NK lysis when added directly to the NK assay. Both drugs also inhibited conjugation of effector cells to target cells. The inhibitory effect of cycloheximide on both the NK lysis and NK activation was reversible while that of emetine was irreversible. Both agents were able to inhibit 3H-amino acid incorporation at the concentrations that inhibited NK activity and activation. Culture-activated NK cells were found to be less susceptible to inhibition by cycloheximide and emetine.
将大鼠脾脏自然杀伤(NK)细胞与51Cr标记的YAC-1或TMT-081肿瘤细胞共同培养18小时,在37℃条件下可增强其活性。蛋白质合成抑制剂放线菌酮和吐根碱,可抑制这种NK细胞的激活,并且当直接添加到NK检测中时,也能抑制NK细胞的杀伤作用。这两种药物还抑制效应细胞与靶细胞的结合。放线菌酮对NK细胞杀伤作用和激活作用的抑制是可逆的,而吐根碱的抑制作用是不可逆的。在抑制NK细胞活性和激活作用的浓度下,这两种药物均能抑制3H-氨基酸掺入。结果发现,经培养激活的NK细胞对放线菌酮和吐根碱的抑制作用不太敏感。