中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2011年
12期
2240-2242
,共3页
何智群%胡卫东%黎春艳%秦毅%吴开松
何智群%鬍衛東%黎春豔%秦毅%吳開鬆
하지군%호위동%려춘염%진의%오개송
肺癌%苦碟子注射液%细胞增殖%细胞凋亡%细胞周期%p53
肺癌%苦碟子註射液%細胞增殖%細胞凋亡%細胞週期%p53
폐암%고설자주사액%세포증식%세포조망%세포주기%p53
Lung cancer%Kudiezi injection%Proliferation%Apoptosis%Cell cycle%p53
目的 探讨苦碟子注射液对人肺癌A549细胞增殖与凋亡的影响及机制.方法 采用噻唑蓝(MTT)比色法、激光共聚焦显微镜(LSM)、流式细胞仪(FCM)及Western blot技术观察12.5 ～400.0 g/L不同浓度苦碟子注射液对A549细胞的增殖、凋亡、细胞周期及p53基因表达的影响.结果 不同浓度KDI对A549细胞增殖均有抑制作用(P＜0.01),50 g/L、100 g/L、200 g/L及400 g/L组细胞凋亡率分别为(12.78±0.29)％、(13.46±0.64)％、(20.52±0.73)％和(13.64±0.21)％,均明显高于对照组的(0.89±0.11)％(P＜0.01),G0/G1期细胞百分比分别为(75.15±1.00)％、(77.52±1.09)％、(79.70±1.48)％和(74.55±0.91)％,均明显高于对照组的(66.28±1.91)％(P＜0.01),A549细胞p53表达量较正常对照组升高(P＜0.05).结论 苦碟子注射液对人肺癌A549细胞有一定的抑制作用,能够诱导人肺癌A549细胞凋亡,可能与其促p53蛋白表达从而阻滞细胞从G1期转向S期有关.
目的 探討苦碟子註射液對人肺癌A549細胞增殖與凋亡的影響及機製.方法 採用噻唑藍(MTT)比色法、激光共聚焦顯微鏡(LSM)、流式細胞儀(FCM)及Western blot技術觀察12.5 ～400.0 g/L不同濃度苦碟子註射液對A549細胞的增殖、凋亡、細胞週期及p53基因錶達的影響.結果 不同濃度KDI對A549細胞增殖均有抑製作用(P＜0.01),50 g/L、100 g/L、200 g/L及400 g/L組細胞凋亡率分彆為(12.78±0.29)％、(13.46±0.64)％、(20.52±0.73)％和(13.64±0.21)％,均明顯高于對照組的(0.89±0.11)％(P＜0.01),G0/G1期細胞百分比分彆為(75.15±1.00)％、(77.52±1.09)％、(79.70±1.48)％和(74.55±0.91)％,均明顯高于對照組的(66.28±1.91)％(P＜0.01),A549細胞p53錶達量較正常對照組升高(P＜0.05).結論 苦碟子註射液對人肺癌A549細胞有一定的抑製作用,能夠誘導人肺癌A549細胞凋亡,可能與其促p53蛋白錶達從而阻滯細胞從G1期轉嚮S期有關.
목적 탐토고설자주사액대인폐암A549세포증식여조망적영향급궤제.방법 채용새서람(MTT)비색법、격광공취초현미경(LSM)、류식세포의(FCM)급Western blot기술관찰12.5 ～400.0 g/L불동농도고설자주사액대A549세포적증식、조망、세포주기급p53기인표체적영향.결과 불동농도KDI대A549세포증식균유억제작용(P＜0.01),50 g/L、100 g/L、200 g/L급400 g/L조세포조망솔분별위(12.78±0.29)％、(13.46±0.64)％、(20.52±0.73)％화(13.64±0.21)％,균명현고우대조조적(0.89±0.11)％(P＜0.01),G0/G1기세포백분비분별위(75.15±1.00)％、(77.52±1.09)％、(79.70±1.48)％화(74.55±0.91)％,균명현고우대조조적(66.28±1.91)％(P＜0.01),A549세포p53표체량교정상대조조승고(P＜0.05).결론 고설자주사액대인폐암A549세포유일정적억제작용,능구유도인폐암A549세포조망,가능여기촉p53단백표체종이조체세포종G1기전향S기유관.
Objective To observe the effect of Kudiezi injection (KDI)on proliferation and apoptosis of human lung cancer cell line A549.Methods After administration of 12.5-400.0 g/L KDI for 24-72 h,the methyl thiazol tetrazolium (MTT) method was used to investigate the inhibitory effect of KDI on A549 cells.Cell apoptosis and cell cycle arrest were investigated by flow cytometry (FCM).Western blot was used to detect the expression of p53 protein.Results KDI significantly inhibit the growth of A549 cancer cells in dose-dependent manners.The number of G0/G1 stage cell was (75.15 ± 1.00)％,(77.52± 1.09) ％,( 79.70 t 1.48 ) ％ and ( 74.55 ± 0.91 ) ％,significant higher than constrol group ( 66.28 ±1.91 )％ (P ＜0.01 ),and that of p53 expression of A549 cancer cells was higher than it in constrol group (P ＜0.05).Conclusion These findings suggest that KDI can inhibit the proliferation of human lung cancer cell line A549 and have obvious dose-effect relationship.The drug inducing people A549 lung cancer cell apoptosis may be relevant to promoting p53 protein expression and its block cells from G1 to S period.
