中华普通外科杂志
中華普通外科雜誌
중화보통외과잡지
CHINESE JOURNAL OF GENERAL SURGERY
2009年
1期
66-70
,共5页
卓志红%张乐鸣%牧启田%楼燕如%施益九%欧阳桂芳%张怡
卓誌紅%張樂鳴%牧啟田%樓燕如%施益九%歐暘桂芳%張怡
탁지홍%장악명%목계전%루연여%시익구%구양계방%장이
胃肿瘤%二十二碳六烯酸类%氟尿嘧啶%细胞凋亡%基因表达
胃腫瘤%二十二碳六烯痠類%氟尿嘧啶%細胞凋亡%基因錶達
위종류%이십이탄륙희산류%불뇨밀정%세포조망%기인표체
Stomach neoplasms%Docosahexaenoic acids%Fluorouracil%Apoptosis%Gene expression
目的 评估二十二碳六烯酸(DHA)联合5氟尿嘧啶(5-Fu)对胃癌细胞SGC 7901生长以及bcl-2、bcl 2l12和bax基因表达的影响.方法 采用台盼蓝拒染方法检测两药物单用和联用对细胞活力的影响,用联合系数判断两药合用效果,倒置显微镜下观察细胞生长状况,PI染色流式细胞术检测亚二倍体峰比并拟合细胞周期曲线,Annexin-V/PI双标记方法检测早期细胞凋亡,RT-PCR方法检测bcl-2、bcl 2l12和bax基因的表达.结果 DHA可抑制胃癌SGC 7901细胞生长,且呈剂量和时间依赖性(P<0.05),24 h、48 h的半数抑制浓度分别为67.81 μg/ml、45.76 μg/ml;DHA联合5-FU对细胞生长的抑制具有协同作用(CI<1,P<0.01),倒置显微镜下可见两药联合处理后细胞稀疏;亚二倍体峰比、Annexin-V早期凋亡率示DHA、5-FU均能诱导细胞凋亡且联合用药后细胞凋亡更明显(DHA、5-FU、联合组的亚二倍体峰比分别为5.2%、6.2%、13.9%;早期细胞凋亡率分别为4.00%、5.37%、13.11%);细胞周期曲线在联合组停滞于G0/G1和S期;RT-PCR显示DHA、5-FU可下调bcl-2和bcl 2l12表达,两药联合表达时下调更显著,bax表达则无明显改变.结论 DHA能抑制胃癌SGC 7901细胞增殖,联合5-FU后对细胞生长抑制和周期阻滞具有协同作用,可能通过下调bcl-2和bcl 2l12基因诱导胃癌SGC 7901细胞发生凋亡.
目的 評估二十二碳六烯痠(DHA)聯閤5氟尿嘧啶(5-Fu)對胃癌細胞SGC 7901生長以及bcl-2、bcl 2l12和bax基因錶達的影響.方法 採用檯盼藍拒染方法檢測兩藥物單用和聯用對細胞活力的影響,用聯閤繫數判斷兩藥閤用效果,倒置顯微鏡下觀察細胞生長狀況,PI染色流式細胞術檢測亞二倍體峰比併擬閤細胞週期麯線,Annexin-V/PI雙標記方法檢測早期細胞凋亡,RT-PCR方法檢測bcl-2、bcl 2l12和bax基因的錶達.結果 DHA可抑製胃癌SGC 7901細胞生長,且呈劑量和時間依賴性(P<0.05),24 h、48 h的半數抑製濃度分彆為67.81 μg/ml、45.76 μg/ml;DHA聯閤5-FU對細胞生長的抑製具有協同作用(CI<1,P<0.01),倒置顯微鏡下可見兩藥聯閤處理後細胞稀疏;亞二倍體峰比、Annexin-V早期凋亡率示DHA、5-FU均能誘導細胞凋亡且聯閤用藥後細胞凋亡更明顯(DHA、5-FU、聯閤組的亞二倍體峰比分彆為5.2%、6.2%、13.9%;早期細胞凋亡率分彆為4.00%、5.37%、13.11%);細胞週期麯線在聯閤組停滯于G0/G1和S期;RT-PCR顯示DHA、5-FU可下調bcl-2和bcl 2l12錶達,兩藥聯閤錶達時下調更顯著,bax錶達則無明顯改變.結論 DHA能抑製胃癌SGC 7901細胞增殖,聯閤5-FU後對細胞生長抑製和週期阻滯具有協同作用,可能通過下調bcl-2和bcl 2l12基因誘導胃癌SGC 7901細胞髮生凋亡.
목적 평고이십이탄륙희산(DHA)연합5불뇨밀정(5-Fu)대위암세포SGC 7901생장이급bcl-2、bcl 2l12화bax기인표체적영향.방법 채용태반람거염방법검측량약물단용화련용대세포활력적영향,용연합계수판단량약합용효과,도치현미경하관찰세포생장상황,PI염색류식세포술검측아이배체봉비병의합세포주기곡선,Annexin-V/PI쌍표기방법검측조기세포조망,RT-PCR방법검측bcl-2、bcl 2l12화bax기인적표체.결과 DHA가억제위암SGC 7901세포생장,차정제량화시간의뢰성(P<0.05),24 h、48 h적반수억제농도분별위67.81 μg/ml、45.76 μg/ml;DHA연합5-FU대세포생장적억제구유협동작용(CI<1,P<0.01),도치현미경하가견량약연합처리후세포희소;아이배체봉비、Annexin-V조기조망솔시DHA、5-FU균능유도세포조망차연합용약후세포조망경명현(DHA、5-FU、연합조적아이배체봉비분별위5.2%、6.2%、13.9%;조기세포조망솔분별위4.00%、5.37%、13.11%);세포주기곡선재연합조정체우G0/G1화S기;RT-PCR현시DHA、5-FU가하조bcl-2화bcl 2l12표체,량약연합표체시하조경현저,bax표체칙무명현개변.결론 DHA능억제위암SGC 7901세포증식,연합5-FU후대세포생장억제화주기조체구유협동작용,가능통과하조bcl-2화bcl 2l12기인유도위암SGC 7901세포발생조망.
Objective To evaluate the growth inhibition of human gastric carcinoma cell lines SGC 7901 in vitro and the expression of bcl-2, bcl 2l12 and bax with docosahexaenoic acid (DHA) and 5-fluorouracil (5-FU). Methods The effect of DHA and 5-FU was measured by trypan blue, and the interaction between two agents was judged by combination index (CI). Cells were observed by inverted microscope. Flow cytometry was used for analysis of apoptosis by PI staining and Annexin-V/PI. RT-PCR was used to analyze the levels of bcl-2, bcl 2l12 and bax mRNA. Results DHA significantly inhibited the growth of SGC 7901 cells in a dose- and time-dependent way ( P < 0. 05 ), the IC50 of 24 h and 48 h was 67. 81 μg/ml and 45.76 μg/ml, and a strong synergism was found in the combination of DHA and 5-FU (CI < 1 ,P <0. 01 ). Treated by DHA and 5-FU for 48 h, cells became sparse under inverted microscope. DHA or 5-FU was able to induce apoptosis and the effect became even more significant by the combination of DHA and 5-FU. Cells were holted in phase of G01/G1 and S. RT-PCR showed that DHA or 5-FU down-regulated the expression of bcl-2 and bcl 2l12 mRNA, while bax mRNA expression was not downregnlated. Conclusions DHA could inhibit the growth of gastric carcinoma cells, DHA and 5-FU had synergetic effect in the inhibition of the cells growth and blockage of the cell cycles possibly by down-regulating the expression of bcl-2 and bcl 2l12.
