广东医学
廣東醫學
엄동의학
GUNAGDONG MEDICAL JOURNAL
2014年
10期
1487-1490
,共4页
李福娟%唐小云%桂金秋%王小花%李玉婷%张涛%石学魁
李福娟%唐小雲%桂金鞦%王小花%李玉婷%張濤%石學魁
리복연%당소운%계금추%왕소화%리옥정%장도%석학괴
红花注射液%人肝癌细胞株HepG-2%细胞增殖%细胞凋亡%AKT
紅花註射液%人肝癌細胞株HepG-2%細胞增殖%細胞凋亡%AKT
홍화주사액%인간암세포주HepG-2%세포증식%세포조망%AKT
safflower injection%HepG-2%cell proliferation%cell apoptosis%AKT
目的:探讨红花注射液对肝癌HepG-2细胞增殖的影响及分子机制。方法应用红花注射液(0、50、150、250 g/L)处理HepG-2细胞,经AnnexinⅤ-FITC/PI双染荧光显微镜观察细胞凋亡的形态学改变,实时荧光定量PCR检测AKT mRNA表达,蛋白质印迹( Western blot )检测AKT、p-AKT蛋白表达。结果50、150、250 g/L的红花注射液作用于HepG-2细胞48 h后,荧光显微镜下呈现典型的凋亡细胞形态;细胞内AKT mRNA表达水平显著降低,AKT、p-AKT蛋白表达水平也显著下调,且变化趋势均呈一定的剂量依赖关系。结论红花注射液可能通过抑制AKT信号通路,阻碍肝癌HepG-2细胞的增殖及诱导凋亡。
目的:探討紅花註射液對肝癌HepG-2細胞增殖的影響及分子機製。方法應用紅花註射液(0、50、150、250 g/L)處理HepG-2細胞,經AnnexinⅤ-FITC/PI雙染熒光顯微鏡觀察細胞凋亡的形態學改變,實時熒光定量PCR檢測AKT mRNA錶達,蛋白質印跡( Western blot )檢測AKT、p-AKT蛋白錶達。結果50、150、250 g/L的紅花註射液作用于HepG-2細胞48 h後,熒光顯微鏡下呈現典型的凋亡細胞形態;細胞內AKT mRNA錶達水平顯著降低,AKT、p-AKT蛋白錶達水平也顯著下調,且變化趨勢均呈一定的劑量依賴關繫。結論紅花註射液可能通過抑製AKT信號通路,阻礙肝癌HepG-2細胞的增殖及誘導凋亡。
목적:탐토홍화주사액대간암HepG-2세포증식적영향급분자궤제。방법응용홍화주사액(0、50、150、250 g/L)처리HepG-2세포,경AnnexinⅤ-FITC/PI쌍염형광현미경관찰세포조망적형태학개변,실시형광정량PCR검측AKT mRNA표체,단백질인적( Western blot )검측AKT、p-AKT단백표체。결과50、150、250 g/L적홍화주사액작용우HepG-2세포48 h후,형광현미경하정현전형적조망세포형태;세포내AKT mRNA표체수평현저강저,AKT、p-AKT단백표체수평야현저하조,차변화추세균정일정적제량의뢰관계。결론홍화주사액가능통과억제AKT신호통로,조애간암HepG-2세포적증식급유도조망。
Objective To investigate the effect and mechanism of Safflower injection on cell proliferation of human hepatoma cells HepG-2 in vitro.Methods HepG-2 cells were treated by different concentrations (0, 50, 150, 250 g/L) of safflower injection .Fluorescence microscopy was applied to test the morphological changes of apoptosis by AnnexinⅤ-FITC/PI staining.Quantitative real-time PCR was carried to assess the mRNA expression of AKT.Western blot were used to observe the protein expression levels of AKT and p -AKT in HepG-2 cells.Results After treated with Safflower injection , HepG-2 cells presented the typical modality of early apoptosis; with significantly dose -dependent down-regulation in AKT mRNA, and AKT and p-AKT proteins.Conclusion Safflower injection inhibits cell prolifera-tion and induces apoptosis in HepG -2 cells through AKT signaling pathway .