中文摘要：

目的探讨没食子儿茶素没食子酸酯（EGCG）诱导人肝癌细胞株凋亡的作用和机制。方法以不同浓度EGCG处理人肝癌细胞株HepG2和SNNC-7721细胞24h和48h。四甲基偶氮唑蓝比色法和锥虫蓝染色细胞计数评价细胞生长情况；流式细胞术检测细胞凋亡和环氧合酶-2（COX-2）、Bcl-2蛋白；比色法测定天冬氨酸蛋白酶-9和caspase-3活性；RT—PCR检测COX-2和Bcl-2家族mRNA的表达。结果EGCG（50、100、200、400μg／ml）处理48h后，HepG2细胞活性下降至93．8％±2．8％，62．3％±5．4％，33．9％±2．5％和17．6％±3．2％，与对照组（100．0％±2．8％）比较差异均有统计学意义（均P〈0．05）；SNNC-7721细胞活性下降至49．6％±3．5％，30．3％±3．8％，17．7％±2．2％和13．0％±2．5％，与对照组（100．0％±0．8％）比较差异均有统计学意义（均P〈0．05）；100μg／ml EGCG处理细胞24、48、72和96h后，HepG2活细胞计数（×10^4）分别是8．0±1．5，22．0±3．1，37．0±5．4和61．0±8．7，与对照组（15．0±2．5，45．0±5．3，86．0±11．0和210．0±23．0）相比明显减少，差异均有统计学意义（均P〈0．05）；SMNC-7721活细胞计数（×10^4）分别是7．0±2．2,13．0±2．5，20．0±3．7和31．0±4．0，与对照组（14．0±2．2，40．0±4．3，75．0±8．8和182．0±28．0）相比明显减少，差异均有统计学意义（均P〈0．05）。EGCG（50、100、200μg／ml）处理细胞12h后，HepG2细胞凋亡率分别是8．7％±0．4％，18．1％±1．1％和22．1％±1．8％；SNMC-7721细胞凋亡率分别是5．9％±0．3％，7．8％±0．6％和12．2％±0．8％，与对照组（3．3％±0．3％）和（3．7％±0．4％）比较，差异均有统计学意义（P〈0．05）；EGCG（100、200μg／ml）处理细胞12h后，HepG2细胞caspase--9活性为1．8±0．4和2．5±0．4；caspase-3活性为2．0±0．4和2．8±0．5，两者与对照组（1．

英文摘要：

Objective To investigate the effects of epigallocatechin-3-gallate （EGCG） on human hepatocellular carcinoma （HCC） cells and mechanism thereof. Method Human HCC cells of the lines He pG2 and SMMC-7721 were cultured and treated with of EGCG of the concentrations of 6. 25, 12. 5, 25, 50, 100,200, and 400 μg/ml respectively for 24 h and 48 h. The cell viability was assessed by 3-（4, 5- dimethylthiazol-2-yl）-2, 5-diphenyl tetrazolium bromide （MTT） assay. Trypan blue staining was used to count the cells. Flow cytometry was conducted to detect the cell apoptosis. The protein levels of Bcl-2, an anti-apeptosis factor, and cyclooxygenase-2 （COX-2）, an up-regulator of Bcl-2. The activities of caspase-9 and easpase-3 hat promote the apoptosis of HCC cells, were measured using colorimetric method. RT-PCR was used to detect the mRNA expression of COX-2 and Bcl-2 family. Results The viabihties of the HepG2 and SMMC-7721 cells treated with EGCG of the concentrations of 50 - 400 μg/ml for 48 h reduced to 93.8% ±2. 8% , 62. 3% ± 5.4%, 33. 9% ± 2. 5%, and 17.6% ± 3.2% respectively, all significantly lower than that of the control group [ （ 100.0% ±2.8% ）, all P 〈0.05] ; and the viabilities of the SMMC- 772 cells treated with EGCG of the concentrations of 50 -400 μg/ml for 48 h reduced to 49. 6% ± 3.5%, 30. 3% ± 3.8%, 17.7% ± 2. 2%, and 13.0% ± 2. 5% respectively, all significantly lower than that of the control group [ （ 100. 0% ±0. 8% ）, all P 〈0. 05]. After treatment with 100 μg,/ml EGCG for 24 h, 48 h, 72h, and 96 h, the live HepG2 cell numbers were （8.0±1.5）, （22.0±3.1）, （37.0±5.4）, and （61.0 ±8. 7 ） 104 respectively, all significantly lower than those of the control cells [ （ 15.0 ± 2. 5 ）, （45.0 ±5.3）, （86.0 ± 11.0）, and （210. 0 ±23. 0） 104 respectively, all P 〈0. 05] ; and the live SMMC- 7721 cell numbers were （7. 0 ±2.2）, （13. 0 ±2. 5）, （20. 0 ±3.7）, and （31.0 ±4.0） 104 respectively, all significantly lower than thos