Objective: To study the exact role of IGF-I in the development of glioma and the effective target for gene therapyrnagainst brain tumor. Methods: (1)An antisense IGF-I mRNA strategy was performed in rat C6 glioblastoma cells with lipo-rnfectamine assay. The levels of IGF-I expression and cell proliferative potential before and after transfection were compared.rn(2) A rodent animal model (Wist ar rat ) beating subcutaneous C6 tumor was set up, through which the different biologicrncharacters before and after the gene treatment of antisense IGF-I were analyzed. Results: Compared with their parental cells,rnthe transfected C6 cells that expressed IGF-I on a relative low level cut down their proliferative potential about 35 %. (2)rnWithin 8 weeks,the tumors treated with antisense IGF-I disappeared completely,while those in control group became largerncontinuously. Around the tumors,apoptotic cells and mononuclear lymphocytes increased and the IGF-I expression and cellrnproliferative potential decreased in the therapeutic group. Conclusion:The antisense IGF-I mRNA strategy might be a soundrntherapeutic modality against neoplasms. Its mechanism based not only on the antisense-mediate inhibition of IGF-I expres-rnsion but also on the antisense-mediate enhancement of immune response of the host.%目的：明确IGF-1在肿瘤发生发展中的作用，为基因治疗优选靶的。方法：(1)转染含反义IGF-1cDNArn的表达型质粒至鼠C6胶质瘤细胞，对比转染前后细胞IGF-1的表达、增殖活性等变化。(2)对Wistar大鼠-C6胶质rn瘤动物模型实施反义IGF-1基因治疗，对比治疗与否肿瘤大小、IGF-1表达、淋巴细胞浸润等的差别。结果：(1)含rn反义质粒的C6细胞系IGF-1表达减低，增殖活性下降约35％。(2)反义IGF-1治疗后的肿瘤8周内完全消失，而rn对照组持续增大。治疗组肿瘤的凋亡细胞、淋巴细胞浸润增加，IGF-1表达、细胞增殖活性下降。结论：反义IGF-1rn基因转染能有效抑制C6胶质瘤的体内外增殖，增殖活性下降和免疫系统攻击可能是双重原因。
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