中医药信息
中醫藥信息
중의약신식
Information on Traditional Chinese Medicine
2015年
6期
9-12
,共4页
人参皂苷Rd%人脑胶质瘤%增殖%凋亡
人參皂苷Rd%人腦膠質瘤%增殖%凋亡
인삼조감Rd%인뇌효질류%증식%조망
Ginsenoside Rd%Human glioma%Proliferation%Apoptosis
目的:体外研究人参皂苷Rd(GS-Rd)抑制人脑胶质瘤U251细胞增殖机制.方法:采用MTT法检测GS-Rd对U251细胞增殖情况的影响;采用流式细胞仪观察GS-Rd对U251细胞周期及凋亡影响;通过实时荧光定量PCR检测GS-Rd对U251细胞相关凋亡基因表达的影响.结果:1)GS-Rd在浓度为20~80μmol/L范围内对U251细胞均有一定的抑制作用,并且抑制强度随药物浓度的增加而增大,呈剂量依赖性;2)GS-Rd各剂量组均可诱导U251细胞凋亡.细胞周期分析显示随着给药浓度增加,越多的U251细胞被阻滞在G1/G0期,使进入S和G2/M期的细胞减少;3)与空白对照组相比,GS-Rd各剂量组Bcl-2mRNA表达显著降低(P<0.05),同时Caspase-3mRNA表达显著提高(P<0.05).结论:人参皂苷Rd能抑制人脑胶质瘤U251细胞增殖,同时能诱导细胞凋亡,其抑瘤机制可能与下调Bcl-2mRNA表达和上调Caspase-3mRNA表达有关.
目的:體外研究人參皂苷Rd(GS-Rd)抑製人腦膠質瘤U251細胞增殖機製.方法:採用MTT法檢測GS-Rd對U251細胞增殖情況的影響;採用流式細胞儀觀察GS-Rd對U251細胞週期及凋亡影響;通過實時熒光定量PCR檢測GS-Rd對U251細胞相關凋亡基因錶達的影響.結果:1)GS-Rd在濃度為20~80μmol/L範圍內對U251細胞均有一定的抑製作用,併且抑製彊度隨藥物濃度的增加而增大,呈劑量依賴性;2)GS-Rd各劑量組均可誘導U251細胞凋亡.細胞週期分析顯示隨著給藥濃度增加,越多的U251細胞被阻滯在G1/G0期,使進入S和G2/M期的細胞減少;3)與空白對照組相比,GS-Rd各劑量組Bcl-2mRNA錶達顯著降低(P<0.05),同時Caspase-3mRNA錶達顯著提高(P<0.05).結論:人參皂苷Rd能抑製人腦膠質瘤U251細胞增殖,同時能誘導細胞凋亡,其抑瘤機製可能與下調Bcl-2mRNA錶達和上調Caspase-3mRNA錶達有關.
목적:체외연구인삼조감Rd(GS-Rd)억제인뇌효질류U251세포증식궤제.방법:채용MTT법검측GS-Rd대U251세포증식정황적영향;채용류식세포의관찰GS-Rd대U251세포주기급조망영향;통과실시형광정량PCR검측GS-Rd대U251세포상관조망기인표체적영향.결과:1)GS-Rd재농도위20~80μmol/L범위내대U251세포균유일정적억제작용,병차억제강도수약물농도적증가이증대,정제량의뢰성;2)GS-Rd각제량조균가유도U251세포조망.세포주기분석현시수착급약농도증가,월다적U251세포피조체재G1/G0기,사진입S화G2/M기적세포감소;3)여공백대조조상비,GS-Rd각제량조Bcl-2mRNA표체현저강저(P<0.05),동시Caspase-3mRNA표체현저제고(P<0.05).결론:인삼조감Rd능억제인뇌효질류U251세포증식,동시능유도세포조망,기억류궤제가능여하조Bcl-2mRNA표체화상조Caspase-3mRNA표체유관.
Objective:To investigate the inhibitory effects of Ginsenoside Rd on the proliferation of U251 cells in vitro.Methods:The proliferation activity was detected by MTT assay.Cell apoptosis and the change in the cycle of U251 were detected by flow cytometry.Real-time quantitative PCR was used to measure the expres-sion of Bcl-2 and caspase-3 in different groups.Results: The proliferation of U251 cells was inhibited by Ginsenoside Rd with the concentration of 20~80μmol/L to 80 μmol/L in dose dependent manner.All dose groups of Ginsenoside Rd could induce apoptosis of U251 cell.Cell cycle analysis showed that the increase of Ginsenoside Rd concentration and the proportion of cells in G1/G0 phase were increased, while that of cells in Sand G2/M phases was decreased.Compared with the blank control group, all dose groups of Ginsenoside Rd could significantly enhance the gene expression of Caspase-3 mRNA ( P<0 .05 ) , and could decrease the gene expression of Bcl-2 mRNA(P<0.05).Conclusion: The Ginsenoside Rd can remarkably restrain the multiplication of U251 glioma and promote the cell to apoptosis, and antitumor mechanisms can be related to down-regulating the expression of Bcl-2 mRNA and up-regulating the expression of Caspase-3 mRNA.
