Zhanaeva S Ya, Mel'nikova E V, Trufakin V A, Korolenko T A
Research Institute of Physiology, Siberian Division of the Russian Academy of Medical Sciences; Research Institute of Clinical and Experimental Lymphology, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk, Russia.
Bull Exp Biol Med. 2013 Nov;156(1):86-90. doi: 10.1007/s10517-013-2284-0.
We analyzed activities of lysosomal cystein cathepsins B and L in mouse LS lymphosarcoma and its drug-resistant RLS 40 strain and their correlations with the dynamics of the percentage of cells with fragmented DNA and CD14 (+) phagocytes over 3 days after cyclophosphamide injection. LS regression and inhibition of RLS 40 growth after cyclophosphamide injection were paralleled by an increase in cathepsins B and L activities in tumor tissues. The antitumor effect of cyclophosphamide associated with apoptosis intensity and protease activities were significantly higher in LS. Positive correlations between activities of cathepsins B and L and the LS tissue content of cells with fragmented DNA and CD14 (+) phagocytes and negative correlations thereof with tumor weight were detected. It seems that the increase in cathepsins B and L activities in LS tissues was caused by cyclophosphamide induction of apoptosis and depended on the level of tumor cell infiltration with mononuclear phagocytes.
我们分析了小鼠LS淋巴肉瘤及其耐药RLS 40株中溶酶体半胱氨酸组织蛋白酶B和L的活性，以及它们与环磷酰胺注射后3天内DNA片段化细胞和CD14(+)吞噬细胞百分比动态变化的相关性。环磷酰胺注射后LS的消退和RLS 40生长的抑制与肿瘤组织中组织蛋白酶B和L活性的增加同时出现。环磷酰胺的抗肿瘤作用与细胞凋亡强度和蛋白酶活性相关，在LS中显著更高。检测到组织蛋白酶B和L的活性与DNA片段化细胞和CD14(+)吞噬细胞的LS组织含量呈正相关，与肿瘤重量呈负相关。似乎LS组织中组织蛋白酶B和L活性的增加是由环磷酰胺诱导的细胞凋亡引起的，并取决于单核吞噬细胞对肿瘤细胞的浸润水平。
