中文摘要：

目的探讨重组人p53腺病毒（rAd—p53）对不同内源性p53基因型的肝癌细胞生长、凋亡的影响。方法用rAd—p53感染人肝癌HepG2细胞系（p53野生型）和PLC／PRF／5细胞系（p53突变型），Mqq法检测病毒滴度、感染时间与细胞生长抑制之间的关系，Westernblot法检测外源性p53表达情况，流式细胞仪测定细胞凋亡之间情况。结果MTF法结果显示20MOIrAd—p53感染HepG2和PLC／PRF／5细胞48h后，两种细胞生长抑制率分别为（17．40±3．01）％和（25．60±3．88）％，差异有统计学意义（P〈0．01），并且随着病毒滴度或感染时间的增加，生长抑制效应亦逐渐增强；rAd—p53感染两种细胞后p53蛋白表达均明显增高；20MOIrAd-p53感染后48h，细胞凋亡率分别为（6．24±0．74）％和（8．31±0．69）％，差异有统计学意义（P〈0．01）。结论rAd—p53能显著抑制人肝癌细胞生长，诱导细胞凋亡，并且对p53突变型肝癌细胞作用强于p53野生型肝癌细胞。

英文摘要：

Objective To explore the effect of recombinant human adenovirus p53 （rAd-p53） on hepatic carcino- ma cells with different p53 genetic statuses. Methods Two human hepatocellular carcinoma cell lines with differ- ent p53 genetic statuses, HepG2（WT p53） and PLC/PRF/5 （MT p53）, were infected with recombinant adeno- virus carrying wild-typep53 gene （rAd-p53） with increasing muhiplicities of infection（MOI）. Cell survival was e- valuated by MTT, p53 protein expression was detected by Western blot assay; and cell apoptosis was assayed by flow cytometry. Results MTT showed that cell inhibitory rates of HepG2 and PLC/PRF/5 cells, after 48 b＇s infec- tion with 20 MOI values of cells, were （ 17.40＋ 3.01 ） % and （25.60 ＋ 3.88） % （P 〈 0.01 ）, respectively. The transduetion efficiency were gradually increased as the infection time or virus dosage increased. The expression of p53 protein was significantly increased in both cell lines after infection. After 48h, cell apoptosisw as assayed were （6.24 _＋0.74）% and （8.31 -＋0. 69）% （P 〈0. 01 ）by Flow Cytometry. Conclusion tAd-p53 can greatly inhibit proliferation and induce cell apoptosis. And the therapeutic efficacy of tAd-p53 in wild-type p53 hepatocellular car- cinoma cells is much stronger than that in mutate hepatocellular carcinoma cells.