基础医学与临床
基礎醫學與臨床
기출의학여림상
BASIC MEDICAL SCIENCES AND CLINICS
2010年
1期
59-62
,共4页
赵俊霞%闫永鑫%王彦玲%韩硕%闫蕴力
趙俊霞%閆永鑫%王彥玲%韓碩%閆蘊力
조준하%염영흠%왕언령%한석%염온력
刺五加多糖%小细胞肺癌H446细胞株%G_2/M期阻滞%ERK
刺五加多糖%小細胞肺癌H446細胞株%G_2/M期阻滯%ERK
자오가다당%소세포폐암H446세포주%G_2/M기조체%ERK
acaruhopanax senticosus polysaccharide%small cell lung cancer cell lines (H446)%G_2/M arrest%ERK
目的 研究刺五加多糖(ASPS)对人小细胞肺癌H446细胞G_2/M期阻滞的诱导作用及对ERK信号传导途径的影响.方法 流式细胞技术(FCM)检测H446细胞周期;Western blot分析检测ASPS对ERK、p-ERK蛋白的影响.结果 与对照组相比,各ASPS处理组G_2/M期细胞所占的比例明显增高(P<0.01),G_0/G_1期细胞所占的比例没有差异;加入ERK抑制剂PD98059后,G_2/M期和G_0/G_1期细胞所占的比例与对照组没有差异;p-ERK的量显著高于对照组(P<0.01),而对ERK蛋白表达没有明显影响.结论 ASPS可能通过激活ERK信号转导途径诱导H446细胞发生G_2/M期阻滞.
目的 研究刺五加多糖(ASPS)對人小細胞肺癌H446細胞G_2/M期阻滯的誘導作用及對ERK信號傳導途徑的影響.方法 流式細胞技術(FCM)檢測H446細胞週期;Western blot分析檢測ASPS對ERK、p-ERK蛋白的影響.結果 與對照組相比,各ASPS處理組G_2/M期細胞所佔的比例明顯增高(P<0.01),G_0/G_1期細胞所佔的比例沒有差異;加入ERK抑製劑PD98059後,G_2/M期和G_0/G_1期細胞所佔的比例與對照組沒有差異;p-ERK的量顯著高于對照組(P<0.01),而對ERK蛋白錶達沒有明顯影響.結論 ASPS可能通過激活ERK信號轉導途徑誘導H446細胞髮生G_2/M期阻滯.
목적 연구자오가다당(ASPS)대인소세포폐암H446세포G_2/M기조체적유도작용급대ERK신호전도도경적영향.방법 류식세포기술(FCM)검측H446세포주기;Western blot분석검측ASPS대ERK、p-ERK단백적영향.결과 여대조조상비,각ASPS처리조G_2/M기세포소점적비례명현증고(P<0.01),G_0/G_1기세포소점적비례몰유차이;가입ERK억제제PD98059후,G_2/M기화G_0/G_1기세포소점적비례여대조조몰유차이;p-ERK적량현저고우대조조(P<0.01),이대ERK단백표체몰유명현영향.결론 ASPS가능통과격활ERK신호전도도경유도H446세포발생G_2/M기조체.
Objective To investigate ASPS induced G_2/M arrest in lung cancer cell line H446 and its effect on ERK MAP kinase signal transduction pathways. Methods Cell cycle phases were inspected by flow cytometery (FCM) ; Western blot analysis was used to inspect the proteins of ERK, p-ERK. Results Compared with control group, G_2/M phase cells increased with concentration significantly, G_0/G_1 phase cells were not different, G_2/M phase cells and G_0/G_1 phase cells were not different when pre-incubated with PD98059 prior to exposure to ASPS of different concentrations, protein of p-ERK was significantly increased, expression of ERK was no different. Conclusion ASPS may induce G_2/M arrest of H446 cells possibly by activation ERK MAP kinase pathways.
