山东医药
山東醫藥
산동의약
Shandong Medical Journal
2015年
38期
7-9
,共3页
张剑青%陈美霓%郭巍%赵菊梅%王爱红%庞秋霞
張劍青%陳美霓%郭巍%趙菊梅%王愛紅%龐鞦霞
장검청%진미예%곽외%조국매%왕애홍%방추하
17丙烯胺-17-去甲氧格尔结霉素%热休克蛋白抑制剂%顺铂%肝细胞癌%细胞增殖%细胞凋亡%Bax蛋白%Bcl-2蛋白
17丙烯胺-17-去甲氧格爾結黴素%熱休剋蛋白抑製劑%順鉑%肝細胞癌%細胞增殖%細胞凋亡%Bax蛋白%Bcl-2蛋白
17병희알-17-거갑양격이결매소%열휴극단백억제제%순박%간세포암%세포증식%세포조망%Bax단백%Bcl-2단백
17-AAG%heat-shock proteins inhibitor%cisplatin%hepatocellular carcinoma%cell proliferation%apopto-sis%Bax protein%Bcl-2 protein
目的:观察热休克蛋白90抑制剂17-AAG联合顺铂( DDP)对人肝癌HepG2细胞增殖的影响,并探讨其机制。方法将对数生长期的HepG2细胞分为对照组和A、B、C组。对照组只加培养基。 A组加入0.625μmol/L的17-AAG,B组加入1.0μg/mL的DDP,C组加入0.625μmol/L的17-AAG和1.0μg/mL的DDP。培养24、48 h后用MTT法测算A、B、C组细胞增殖抑制率,用流式细胞术测算各组细胞凋亡率,用RT-PCR法检测各组Bax、Bcl-2 mRNA。结果 A、B、C组培养48 h时细胞增殖抑制率均高于培养24 h时,P均<0.05;培养时间相同时C组细胞增殖抑制率高于A、B组,P均<0.05。培养48 h后A、B、C组细胞凋亡率和Bax mRNA均高于对照组,Bcl-2 mRNA低于对照组,P均<0.05;C组细胞凋亡率和Bax mRNA均高于A、B组,Bcl-2 mRNA低于A、B组,P均<0.05。结论17-AAG对人肝癌HepG2细胞具有生长抑制作用,其与顺铂联合有协同作用。其机制可能与上调细胞Bax mRNA、下调Bcl-2 mRNA表达有关。
目的:觀察熱休剋蛋白90抑製劑17-AAG聯閤順鉑( DDP)對人肝癌HepG2細胞增殖的影響,併探討其機製。方法將對數生長期的HepG2細胞分為對照組和A、B、C組。對照組隻加培養基。 A組加入0.625μmol/L的17-AAG,B組加入1.0μg/mL的DDP,C組加入0.625μmol/L的17-AAG和1.0μg/mL的DDP。培養24、48 h後用MTT法測算A、B、C組細胞增殖抑製率,用流式細胞術測算各組細胞凋亡率,用RT-PCR法檢測各組Bax、Bcl-2 mRNA。結果 A、B、C組培養48 h時細胞增殖抑製率均高于培養24 h時,P均<0.05;培養時間相同時C組細胞增殖抑製率高于A、B組,P均<0.05。培養48 h後A、B、C組細胞凋亡率和Bax mRNA均高于對照組,Bcl-2 mRNA低于對照組,P均<0.05;C組細胞凋亡率和Bax mRNA均高于A、B組,Bcl-2 mRNA低于A、B組,P均<0.05。結論17-AAG對人肝癌HepG2細胞具有生長抑製作用,其與順鉑聯閤有協同作用。其機製可能與上調細胞Bax mRNA、下調Bcl-2 mRNA錶達有關。
목적:관찰열휴극단백90억제제17-AAG연합순박( DDP)대인간암HepG2세포증식적영향,병탐토기궤제。방법장대수생장기적HepG2세포분위대조조화A、B、C조。대조조지가배양기。 A조가입0.625μmol/L적17-AAG,B조가입1.0μg/mL적DDP,C조가입0.625μmol/L적17-AAG화1.0μg/mL적DDP。배양24、48 h후용MTT법측산A、B、C조세포증식억제솔,용류식세포술측산각조세포조망솔,용RT-PCR법검측각조Bax、Bcl-2 mRNA。결과 A、B、C조배양48 h시세포증식억제솔균고우배양24 h시,P균<0.05;배양시간상동시C조세포증식억제솔고우A、B조,P균<0.05。배양48 h후A、B、C조세포조망솔화Bax mRNA균고우대조조,Bcl-2 mRNA저우대조조,P균<0.05;C조세포조망솔화Bax mRNA균고우A、B조,Bcl-2 mRNA저우A、B조,P균<0.05。결론17-AAG대인간암HepG2세포구유생장억제작용,기여순박연합유협동작용。기궤제가능여상조세포Bax mRNA、하조Bcl-2 mRNA표체유관。
Objective To explore the effects of 17-AAG combined with cisplatin ( DDP) on the proliferation of human hepatocellular carcinoma HepG 2 cells and its mechanism .Methods HepG2 cells in the logarithmic phase were divided into the control group and groups A , B and C.The control group was only added with medium .Group A was added with 0.625 μmol/L 17-AAG, group B was added with 1.0 μg/mL DDP, and group C was added with 0.625 μg/mL 17-AAG and 1.0 μg/mL DDP.After being cultured for 24 h and 48 h, the cell proliferation inhibition rates of groups A , B and C were determined by MTT , the apoptosis rate was measured by flow cytometry , and the Bax and Bcl-2 mRNA in each group was measured by RT-PCR.Results The cell proliferation inhibition rates of groups A , B and C which were cultured for 48 h were all higher than those of being cultured for 24 h (all P<0.05), the cell proliferation inhibition rate of group C was higher than those of groups A and B at the same time of culture (all P<0.05).After being cultured for 48 h, the apopto-sis rate and Bax mRNA in the groups A , B and C were higher than that of the control group , while Bcl-2 mRNA was lower than that of the control group (all P<0.05); the apoptosis rate and Bax mRNA of group C were higher than those of groupsAandB,buttheBcl-2mRNAwaslowerthanthoseofgroupsAandB(allP<0.05).Conclusions 17-AAGin-hibits the growth of human hepatocellular carcinoma HepG 2 cells and has synergistic effect with cisplatin .The mechanism may be related to the up-regulation of Bax mRNA and down-regulation of Bcl-2 mRNA expression .