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金诺芬对大鼠外周血多形核白细胞和单核细胞介导的抗体依赖性细胞毒性(ADCC)的影响。

Effect of auranofin on antibody-dependent cellular cytotoxicity (ADCC) mediated by rat peripheral blood polymorphonuclear leukocytes and mononuclear cells.

作者信息

DiMartino M J, Walz D T

出版信息

Inflammation. 1980 Sep;4(3):279-88. doi: 10.1007/BF00915029.

Abstract

Auranofin and other clinically used gold compounds were evaluated in vitro for effects on antibody-dependent cellular cytotoxicity (ADCC) of L929 fibroblast target cells mediated by adjuvant rat peripheral blood PMNs or mononuclear cells. Auranofin (10 microM) was found to be a potent inhibitor of PMNADCC. In contrast, gold sodium thiomalate (10-100 microM), gold thioglucose (10-1000 microM), and nongold substructures of auranofin (10 microM) were not inhibitory.. In continuous culture, gold sodium thiomalate and relatively low concentrations of auranofin (smaller than or equal to microM) significantly enhanced PMNADCC. Results of pretreatment studies indicate that auranofin's inhibitory activity of PMNADCC is caused by a noncytotoxic effect on PMN function which is not associated with alteration of PMN-target cell contact. In contrast to its inhibitory activity on PMNADCC, auranofin pretreatment of mononuclear cells resulted in enhanced target cell destruction which appeared to correlate with increased mononuclear cell-target cell contact.

摘要

对金诺芬及其他临床使用的金化合物进行了体外评估,以研究其对佐剂诱导的大鼠外周血多形核白细胞(PMN)或单核细胞介导的L929成纤维细胞靶细胞抗体依赖性细胞毒性(ADCC)的影响。发现金诺芬(10微摩尔)是PMN-ADCC的有效抑制剂。相比之下,硫代苹果酸金钠(10 - 100微摩尔)、硫代葡萄糖金(10 - 1000微摩尔)以及金诺芬的非金亚结构(10微摩尔)并无抑制作用。在连续培养中,硫代苹果酸金钠和相对低浓度的金诺芬(小于或等于1微摩尔)显著增强了PMN-ADCC。预处理研究结果表明,金诺芬对PMN-ADCC的抑制活性是由对PMN功能的非细胞毒性作用引起的,这与PMN-靶细胞接触的改变无关。与其对PMN-ADCC的抑制活性相反,金诺芬预处理单核细胞导致靶细胞破坏增强,这似乎与单核细胞-靶细胞接触增加相关。

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