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目的 观察阳离子脂质体介导的单纯疱疹病毒胸苷激酶基因 (HSV TK)、野生型P5 3基因 (wt p5 3 )联合治疗裸鼠肝癌的作用。方法 用 6μlDosper脂质体介导将 1.5 μgHSV TK基因、1.5 μg野生型 p5 3基因转染人肝癌细胞系SMMC 772 1,逆转录聚合酶链反应 (RT PCR)检测基因表达 ,四唑蓝比色 (MTT)法测定其对肝癌细胞的杀伤作用。在 0 .8cm裸鼠肝癌模型单独或联合导入 5 μg基因后 ,结合应用前药无氧鸟苷 (GCV ) 10 0mg/kg体重 7～ 10d ,分别观察肿瘤的生长情况。结果 单独导入wt p5 3对肝癌细胞的抑制率为 15 % ,与HSV TK基因联用后 ,在GCV 10μmol/L时 ,杀伤效率明显强于单用HSV TK ,但在GCV 10 0 0 μmol/L时 ,两者间杀伤效率差异无显著性 (P >0 .0 5 )。在裸鼠实验性肝癌 ,导入wt p5 3后 ,肿瘤的生长受到抑制 ;wt p5 3与HSV TK/GCV联用后 ,在治疗的第 8天就有 4只 (80 % )裸鼠肿瘤完全消退 ,与HSV TK/GCV组相比差异有显著性 (P <0 .0 5 )。结论 HSV TK基因、wt p5 3基因联合应用对裸鼠肝癌有显著杀伤作用。
Objective To observe the effect of cationic liposome-mediated HSV TK and wild-type P5 3 gene (wt p5 3) on hepatoma in nude mice. METHODS: Transfection of 1.5 μg of HSV TK gene and 1.5 μg of wild-type p5 3 gene into human hepatocellular carcinoma cell line SMMC 772 1 was induced by 6 μl of liposomal liposome. The gene expression was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) (MTT) method to determine its killing effect on hepatoma cells. Tumor growth was observed in 0 .8 cm nude mouse model of hepatocellular carcinoma either alone or in combination with 5 μg of the gene. The combined use of 100 mg / kg body weight of anoxia-guanosine (GCV) at 10 mg / kg body weight for 7-10 days. Results The wt% inhibition rate of wt p5 3 alone was 15%. When combined with HSV TK gene, the cytotoxicity was significantly higher than that of HSV TK alone at GCV 10 μmol / L, but the GCV at 100 μmol / L , There was no significant difference in the killing efficiency between the two (P> 0.05). In nude mice, the growth of the tumor was inhibited after the introduction of wt p5 3. After wt p5 3 combined with HSV TK / GCV, 4 (80%) nude mice completely regressed on the 8th day of treatment , There was significant difference compared with HSV TK / GCV group (P <0.05). Conclusion The combination of HSV TK gene and wt p5 3 gene can significantly kill hepatocellular carcinoma in nude mice.