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作 者:邓松华[1,2] 汪思应[1,2] 程洁[1,2] 张宝霆 姚立人[1,2] 任伟 王丹[1,2]
机构地区:[1]安徽医科大学病理生理学教研室 [2]安徽省立医院肾内科
出 处:《中国药理学通报》1998年第2期143-144,共2页Chinese Pharmacological Bulletin
基 金:国家自然科学基金
摘 要:目的探讨rIL-2抗肿瘤机制。方法用“LDH释放法”检测经不同处理的脾细胞对其敏感的靶细胞YAC-1,不敏感的lewis肺癌(LLC)及耐受的LLC肺转移细胞(LLCF1)体外杀伤功能。结果正常脾细胞对3种靶细胞的杀伤能力有明显差异(P<0.01);经人rIL-2体外激活后(LAK细胞),杀瘤能力明显增强,并对LLC、LLCF1细胞的杀伤作用已无明显差异;对LLC血道转移也有明显抑制作用;激活时间对脾细胞杀瘤能力也有影响。结论人rIL-2能激活小鼠脾细胞,使其杀瘤尤其是对具有抗NK细胞的肿瘤杀伤能力明显增强,对肿瘤转移也有疗效。AIM To study the antitumor mechnism of human rIL2. METHODS The cytotoxicity against YAC1, LLC, LLCF1 cell of murine splenic cell treated differently is assayed by “lactic acid dehydrogense release” method. RESULTS The cytotoxicities of normal murine splenic cells against three target cells are significantly variant (P<001). After being activated by human rIL2 in vitro (as LAK cell), its antitumor activity increased, especially to LLCF1 cells. Being activated in different time, the cytolysis of LAK cells against targets is various. LAK cells can inhibit the LLC murine experimental pulmonary metastasis in vivo. CONCLUSION These results indicated the LLC murine splenic cells can be activated by human rIL2, and antitumor activity increases, especially to the tumor cell against NK cells. LAK cells are found to be effective in the therapy of LLC lung metastases.
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