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作 者:王金环[1] 房欣[2] 史国利[2] 蔡宝立[2]
机构地区:[1]天津第一中心医院神经外科,天津300192 [2]南开大学分子生物学研究所
出 处:《中国神经精神疾病杂志》2002年第3期169-172,共4页Chinese Journal of Nervous and Mental Diseases
摘 要:目的 为了探讨联合应用单纯疱疹病毒 胸苷激酶和野生型p5 3两种基因治疗胶质瘤的可能性。方法 构建了含CMV启动子和单纯疱疹病毒胸苷激酶基因 (HSV TK)的重组腺病毒AdCMV TK和含CMV启动子及野生型p5 3的重组腺病毒AdCMV p5 3。以感染复数 (MOI)为 1 0 0的病毒剂量 ,用AdCMV TK和AdCMV p5 3同时感染人胶质母细胞瘤细胞系TJ90 5 ,并以 1 0 0MOI的AdCMV TK和AdCMV p5 3分别感染另外两组TJ90 5细胞。除感染AdCMV p5 3的细胞外 ,其他两组均于感染后加入 1 0 0 μmol/LGCV。 结果 感染AdCMV p5 3的TJ90 5细胞 ,其生长受到抑制 ,于感染后第 5d,细胞存活率下降为 3 6 9% ,感染AdCMV TK的细胞 ,其生长抑制程度与感染AdCMV p5 3的TJ90 5细胞相似 ,用药后第 5d ,细胞存活率为 3 0 1 % ,而同时感染两种重组腺病毒的细胞 ,细胞生长的抑制程度更明显 ,应用 1 0 0μmol/LGCV后第 5d,细胞存活率仅为 8 8%。结论 联合应用AdCMV TK和AdCMV p5Objective To investigate the feasibility of combining HSV TK with wild p53 for gene therapy of glioma. Methods Two recombinant adenovirus were constructed. Those were AdCMV TK that contained CMV promoter and herpes simplex virus thymidine gene (HSV TK) and AdCMV p53 that contained CMV promoter and wild p53 gene. Human glioblastoma cell line (TJ905) was infected with both of AdCMV TK and AdCMV p53 in 100 of multiplicity of infection(MOI). The other two groups of TJ905 were infected with AdCMV TK and AdCMV p53 in 100MOI respectively. Except for the group of AdCMV p53, the other two groups were treated with 100 μM GCV.Results Proliferation of TJ905 cells infected with AdCMV p53 was inhibited and the cell survival rate decreased to 36.9% in the 5 day after infected. Proliferation of cells infected with AdCMV TK was similar to that of cells infected with AdCMV p53. The cell survival rate was 30.1% in the day 5 after GCV was used. Proliferation of cells infected with both of AdCMV TK and AdCMV p53 was significantly inhibited. After GCV was used, the cell survival rate decreased to 8.8% in day 5. Conclusions Combining AdCMV TK and AdCMV p53 for gene therapy of glioma is a valuable method.
关 键 词:体外实验 单纯疱疹病毒-胸苷激酶 野生型P53基因 重组腺病毒 pACCMV AdCMV-p53 胸胶质瘤 脑肿瘤 基因治疗
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