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机构地区:[1]同济医科大学医学分子生物学研究室,武汉430030
出 处:《中国肿瘤生物治疗杂志》2000年第1期28-31,共4页Chinese Journal of Cancer Biotherapy
基 金:国家自然科学基金!(39870763);国家教委跨世纪人才培养计划基金资助
摘 要:目的:研究重组FN多肽CH50在体内激活巨噬细胞及其抗肿瘤作用的特点。方法:体内注射CH50和/或转染IFN-γ基因,检测巨噬细胞产生的各种因子,测定荷瘤鼠体内肿瘤生长速度。结果:CH50单独作用可促进巨噬细胞产生NO,TNF,IL-1等因子,但激活作用较慢。注射CH50和转染IFN-γ基因不分先后,均可在体内协同作用,迅速激活巨噬细胞。单独注射CH50能够抑制肿瘤结节的形成,其抑制作用呈剂量依赖关系;低剂量CH60对<1mm的肿瘤结节已有很强的抑制作用,较大剂量时对>1mm的肿瘤结节也有很强的抑制作用。CH50与IFN-了在体内的协同作用使其抑制体内肿瘤生长的作用更强。结论:CH50与IFN-γ作为体内巨噬细胞激活的双信号因子在肿瘤治疗中具有极大的应用潜力。Objective: To study the main features of CH50, a recombinant polypeptide of human fibronectin, to activate macrophages in vivo and its anti-tumor function. Methods: CH50 was injected and IFN-γ gene was transfected in mice several kinds of factors produced by marcrophages were determined. The growth of tumor in force was also measured. Results: CH50 could enhance the production of such factors as NO, TNF and IL-1 by macrophages, but the activation of macrophages was rela- tively slow when CH50 was used in vivo alone. CH50 and IFN-γ could synergistically activate macrophages rapidly in vivo no matter whether the injection of CH50 or the transfection of IFN-γ gene was Performed first.Injection of CH50 alone inhibited the formation of tumor nodes in a dose-dependent manner. There was strong inhibition of low dosage of CH50 on the formation of tu- mor nodes smaller than 1 mm, and high dosage of CH50 on those bigger than 1 mm. A stronger inhibition on the growth of tumor in vivo was obtained by the synergistic effect of CH50 and IFN-γ. Conclusion: CH50 and IFN-γ, as double-signal factors for activation of macrophages, will be potentially useful in tumor therapy.
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