诱导肺泡巨噬细胞分泌细胞毒因子抑制小鼠黑色素瘤肺转移  被引量:2

INHIBITION OF LUNG METASTASIS OF A MOUSE MELANOMA BY INDUCING RELEASE OF CYTOTOXIC FACTORS FROM ACTIVATED ALVEOLAR MACROPHAGES

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作  者:任园[1] 张友会[1] 

机构地区:[1]中国医学科学院中国协和医科大学肿瘤研究所

出  处:《中国免疫学杂志》1998年第6期431-433,共3页Chinese Journal of Immunology

摘  要:以腹腔注射卡介苗或康赛宁,再雾化吸入rIL-2,来抑制小鼠黑色素瘤B16-BL6细胞的肺转移。结果表明,小鼠肺转移被显著抑制,抑制率最高达78.95%,小鼠生存期最多延长了48.20%;腹腔注射N-单甲基-L-精氨酸(NMA)使抑制作用显著减弱,平均下降了69.00%。体外实验证明,B16-BL6细胞对NO的细胞毒作用敏感,对TNF不敏感。结果显示,肺转移的抑制作用可能主要是活化的肺泡巨噬细胞分泌的NO介导的。在活化肺泡巨噬细胞基础上雾化吸入rIL-2,不失为治疗肿瘤肺转移的另一途径。BCG or kanserin was injected ip to systemically activate macrophages in C57BL/6 mice.The activated alveolar macrophages were triggered to release cytotoxic factors by aerosolized rIL 2 inhalation.The results showed that experimental lung metastasis was marked inhibited in the treated mice.The inhibitory rate of metastasis was 78.95% and the surviving time of the treated mice increased by 48.20%.The anti metastatic activity could be markedly abrogated by ip injection of NO synthase inhibitor N G monomethly L arginine,leading to a 69.00% decrease in anti metastatic activity.Experiments in vitro confirmed that B16 BL6 was sensitive to NO mediated cytotoxicity but resistant to TNF.The results indicated that the inhibitory effect on pulmonary metastasis is mainly mediated via NO from activated alveolar macrophages.Inhalation of aerosolized rIL 2 following activation of alveolar macrophages may after all be a novel approach in the treatment of pulmonary metastasis.

关 键 词:肺泡巨噬细胞 一氧化氮 黑色素瘤 肺转移 肺肿瘤 

分 类 号:R734.203[医药卫生—肿瘤] R739.5[医药卫生—临床医学]

 

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