中华胰腺病杂志
中華胰腺病雜誌
중화이선병잡지
CHINESE JOURNAL OF PANCREATOLOGY
2011年
2期
101-103
,共3页
彭凯%孔心涓%田字彬%张翠萍%赵清喜%魏良洲%王斌
彭凱%孔心涓%田字彬%張翠萍%趙清喜%魏良洲%王斌
팽개%공심연%전자빈%장취평%조청희%위량주%왕빈
胰腺肿瘤%表没食子儿茶素没食子酸酯%细胞凋亡%细胞周期
胰腺腫瘤%錶沒食子兒茶素沒食子痠酯%細胞凋亡%細胞週期
이선종류%표몰식자인다소몰식자산지%세포조망%세포주기
Pancreatic neoplasms%Epigalocatechin-3 gallate%Apoptosis%Cell cyle
目的 探讨表没食子儿茶素没食子酸酯(EGCG)对人胰腺癌细胞株SW1990增殖及细胞凋亡、细胞周期的影响.方法 采用四甲基偶氮唑蓝(MTT)比色法检测不同浓度EGCG(6.25、12.5、25、50、100μg/ml)对体外培养的SW1990细胞增殖的影响;采用流式细胞仪检测EGCG(25μg/ml)对SW1990细胞凋亡及不同浓度的EGCG(0、10、20、30、40、50 μg/ml)对SW1990细胞周期的影响.结果 不同浓度EGCG(0、25、50μg/ml)作用SW1990细胞24 h后,吸光度值(A492)分别为0.46±0.04、0.42±0.04、0.27±0.03,48 h后分别为0.48±0.02、0.31±0.03、0.16±0.02,72 h后分别为0.51±0.01、0.24±0.04、0.14±0.04,EGCG呈浓度及时间依赖性抑制SW1990的增殖(P<0.01).25 μg/ml EGCG作用于SW1990细胞24、48、72 h后的细胞凋亡率分别为(8.33±1.15)%、(19.77±0.81)%、(29.17±0.75)%,而对照组相应的细胞凋亡率分别为(2.77±0.45)%、(3.20±0.26)%、(3.67±0.35)%,两组差异具有统计学意义(P<0.01).0、20、50 μg/ml EGCG作用SW1990细胞24 h后,G0/G1期细胞分别占(57.59±0.97)%、(62.99±1.91)%、(68.87±1.88)%,随着EGCG浓度的增加,Go/G1期细胞比例明显增加,而S期和G2/M期细胞比例相应下降(P<0.01).结论 EGCG能明显抑制SW1990细胞的增殖,其机制可能与其诱导SW1990细胞凋亡及调控细胞周期有关.
目的 探討錶沒食子兒茶素沒食子痠酯(EGCG)對人胰腺癌細胞株SW1990增殖及細胞凋亡、細胞週期的影響.方法 採用四甲基偶氮唑藍(MTT)比色法檢測不同濃度EGCG(6.25、12.5、25、50、100μg/ml)對體外培養的SW1990細胞增殖的影響;採用流式細胞儀檢測EGCG(25μg/ml)對SW1990細胞凋亡及不同濃度的EGCG(0、10、20、30、40、50 μg/ml)對SW1990細胞週期的影響.結果 不同濃度EGCG(0、25、50μg/ml)作用SW1990細胞24 h後,吸光度值(A492)分彆為0.46±0.04、0.42±0.04、0.27±0.03,48 h後分彆為0.48±0.02、0.31±0.03、0.16±0.02,72 h後分彆為0.51±0.01、0.24±0.04、0.14±0.04,EGCG呈濃度及時間依賴性抑製SW1990的增殖(P<0.01).25 μg/ml EGCG作用于SW1990細胞24、48、72 h後的細胞凋亡率分彆為(8.33±1.15)%、(19.77±0.81)%、(29.17±0.75)%,而對照組相應的細胞凋亡率分彆為(2.77±0.45)%、(3.20±0.26)%、(3.67±0.35)%,兩組差異具有統計學意義(P<0.01).0、20、50 μg/ml EGCG作用SW1990細胞24 h後,G0/G1期細胞分彆佔(57.59±0.97)%、(62.99±1.91)%、(68.87±1.88)%,隨著EGCG濃度的增加,Go/G1期細胞比例明顯增加,而S期和G2/M期細胞比例相應下降(P<0.01).結論 EGCG能明顯抑製SW1990細胞的增殖,其機製可能與其誘導SW1990細胞凋亡及調控細胞週期有關.
목적 탐토표몰식자인다소몰식자산지(EGCG)대인이선암세포주SW1990증식급세포조망、세포주기적영향.방법 채용사갑기우담서람(MTT)비색법검측불동농도EGCG(6.25、12.5、25、50、100μg/ml)대체외배양적SW1990세포증식적영향;채용류식세포의검측EGCG(25μg/ml)대SW1990세포조망급불동농도적EGCG(0、10、20、30、40、50 μg/ml)대SW1990세포주기적영향.결과 불동농도EGCG(0、25、50μg/ml)작용SW1990세포24 h후,흡광도치(A492)분별위0.46±0.04、0.42±0.04、0.27±0.03,48 h후분별위0.48±0.02、0.31±0.03、0.16±0.02,72 h후분별위0.51±0.01、0.24±0.04、0.14±0.04,EGCG정농도급시간의뢰성억제SW1990적증식(P<0.01).25 μg/ml EGCG작용우SW1990세포24、48、72 h후적세포조망솔분별위(8.33±1.15)%、(19.77±0.81)%、(29.17±0.75)%,이대조조상응적세포조망솔분별위(2.77±0.45)%、(3.20±0.26)%、(3.67±0.35)%,량조차이구유통계학의의(P<0.01).0、20、50 μg/ml EGCG작용SW1990세포24 h후,G0/G1기세포분별점(57.59±0.97)%、(62.99±1.91)%、(68.87±1.88)%,수착EGCG농도적증가,Go/G1기세포비례명현증가,이S기화G2/M기세포비례상응하강(P<0.01).결론 EGCG능명현억제SW1990세포적증식,기궤제가능여기유도SW1990세포조망급조공세포주기유관.
Objective To investigate the apoptosis-inducing effect and anti-proliferative effect of epigallocatechin-3-gallate (EGCG) on human pancreatic cancer cell SW1990 in vitro. Methods The effect of proliferation was evaluated by MTT after the SW1990 cells in vitro were incubated with different concentrations of EGCG (6.25, 12.5, 25, 50, 100 μg/ml). The apoptosis-inducing effect was determined by flow cytometry after the cells were treated with 25 μg/ml of EGCG. The cell cycle of SW1990 cells was detected by flow cytometry after the cells incubated with different concentrations of EGCG (0, 10, 20, 30, 40, 50 μg/ml).Results After SW1990 cell were treated with different concentrations of EGCG (0, 25, 50 μg/ml), the values of A492 were 0.46 ±0.04,0.42 ±0.04,0.27 ±0.03 at 24 h; 0.48 ±0.02, 0.31 ±0.03,0.16 ±0.02at 48 h; 0.51 ±0.01,0.24 ±0.04,0. 14 ±0.04 at 72 h. EGCG inhibited the proliferation of SW1990 in a doseand time-dependant manner(P <0.01 ). The apoptotic rates at 24, 48, 72 h were (8.33 ± 1.15 )%, (19.77 ±0.81 )%, (29.17 ± 0.75 )% in the EGCG treatment group; while the corresponding values were (2.77 ±0.45 ) %, (3.20 ± 0.26 ) %, (3.67 ± 0.35 ) % in the control group; and the difference was statistically significant (P <0.01 ). After 0, 20, 50 μg/ml of EGCG treatment for 24 h, the percentages of SW1990 cellsin G0/G1 stage were (57.59 ±0.97)%, (62.99 ± 1.91 )%, (68.87 ± 1.88)%, and the percentages of SW1990 cells in G0/G1 stage increased with the increase of concentrations of EGCG, while the percentages of SW1990 cells in G2/M stage decreased with the increase of concentrations of EGCG (P <0.01 ). Conclusions EGCG can significantly inhibit the proliferation of SW1990 cells. The mechanism may be related to the apoptosis-inducing effect and the regulation of the cell cycle of the SW1990 cells.