肿瘤药学
腫瘤藥學
종류약학
ANTI-TUMOR PHARMACY
2015年
2期
101-105
,共5页
CXCL12%细胞增殖%VEGF%CXCR4%CXCR7%白藜芦醇
CXCL12%細胞增殖%VEGF%CXCR4%CXCR7%白藜蘆醇
CXCL12%세포증식%VEGF%CXCR4%CXCR7%백려호순
CXCL12%Proliferation%VEGF%CXCR4%CXCR7%Resveratrol
目的:探讨白藜芦醇对趋化因子 CXCL12诱导的人胃癌 SGC-7901细胞增殖及其 CXCR4、CXCR7和VEGF mRNA 表达的影响。方法用 CXCL12刺激人胃癌 SGC-7901细胞后,采用 MTT 法检测细胞增殖率;应用RT-PCR 法检测细胞内 CXCR4、CXCR7和 VEGF mRNA 的表达水平。同时观察白藜芦醇对 CXCL12所诱导的人胃癌 SGC-7901细胞增殖率,CXCR4、CXCR7和 VEGF mRNA 表达水平的影响。结果不同浓度的 CXCL12均可以显著促进人胃癌 SGC-7901细胞体外增殖(P<0.001)。CXCL12可显著上调 SGC-7901细胞 CXCR4、CXCR7和VEGF 的 mRNA 表达,而白藜芦醇显著抑制 CXCL12所诱导的胃癌细胞体外增殖和 CXCR4、CXCR7、VEGF mRNA的表达。结论白藜芦醇抑制 CXCL12诱导的胃癌细胞增殖,其机制可能与下调 CXCR4和 CXCR7水平,从而抑制VEGF 分泌有关。
目的:探討白藜蘆醇對趨化因子 CXCL12誘導的人胃癌 SGC-7901細胞增殖及其 CXCR4、CXCR7和VEGF mRNA 錶達的影響。方法用 CXCL12刺激人胃癌 SGC-7901細胞後,採用 MTT 法檢測細胞增殖率;應用RT-PCR 法檢測細胞內 CXCR4、CXCR7和 VEGF mRNA 的錶達水平。同時觀察白藜蘆醇對 CXCL12所誘導的人胃癌 SGC-7901細胞增殖率,CXCR4、CXCR7和 VEGF mRNA 錶達水平的影響。結果不同濃度的 CXCL12均可以顯著促進人胃癌 SGC-7901細胞體外增殖(P<0.001)。CXCL12可顯著上調 SGC-7901細胞 CXCR4、CXCR7和VEGF 的 mRNA 錶達,而白藜蘆醇顯著抑製 CXCL12所誘導的胃癌細胞體外增殖和 CXCR4、CXCR7、VEGF mRNA的錶達。結論白藜蘆醇抑製 CXCL12誘導的胃癌細胞增殖,其機製可能與下調 CXCR4和 CXCR7水平,從而抑製VEGF 分泌有關。
목적:탐토백려호순대추화인자 CXCL12유도적인위암 SGC-7901세포증식급기 CXCR4、CXCR7화VEGF mRNA 표체적영향。방법용 CXCL12자격인위암 SGC-7901세포후,채용 MTT 법검측세포증식솔;응용RT-PCR 법검측세포내 CXCR4、CXCR7화 VEGF mRNA 적표체수평。동시관찰백려호순대 CXCL12소유도적인위암 SGC-7901세포증식솔,CXCR4、CXCR7화 VEGF mRNA 표체수평적영향。결과불동농도적 CXCL12균가이현저촉진인위암 SGC-7901세포체외증식(P<0.001)。CXCL12가현저상조 SGC-7901세포 CXCR4、CXCR7화VEGF 적 mRNA 표체,이백려호순현저억제 CXCL12소유도적위암세포체외증식화 CXCR4、CXCR7、VEGF mRNA적표체。결론백려호순억제 CXCL12유도적위암세포증식,기궤제가능여하조 CXCR4화 CXCR7수평,종이억제VEGF 분비유관。
Objective To study the effects of resveratrol on the CXCL12-induced proliferation of gastric cancer cell line SGC-7901 and mRNA expression of CXCR4, CXCR7 and VEGF. Methods SGC-7901 cells were treated with CXCL12 and res-veratrol, then the proliferation of the SGC-7901 cells were tested by MTT. The levels of CXCR4, CXCR7 and VEGF mRNA were measured by reverse transcription-polymerase chain reaction (RT-PCR). Results Different concentrations of CXCL12 all sig-nificantly increased the in vitro proliferation of SGC-7901 cells (P<0.001). CXCL12 also up-regulated the mRNA expressions of CXCR4, CXCR7 and VEGF in SGC-7901 cells. We found that resveratrol significantly inhibited CXCL12-induced proliferation of SGC-7901 cells and mRNA expressions of CXCR4, CXCR7 and VEGF. Conclusion Resveratrol could inhibit CXCL12-induced proliferation of gastric cancer cells. The mechanism may be related with the down-regulation of CXCR4, CXCR7 and VEGF levels.