中国癌症杂志
中國癌癥雜誌
중국암증잡지
CHINA ONCOLOGY
2013年
1期
36-41
,共6页
高山%陈秀英%付海燕%崔晓楠
高山%陳秀英%付海燕%崔曉楠
고산%진수영%부해연%최효남
华蟾素注射液%HLEC%增殖%迁移%管状形成%VEGFR-3%HGF
華蟾素註射液%HLEC%增殖%遷移%管狀形成%VEGFR-3%HGF
화섬소주사액%HLEC%증식%천이%관상형성%VEGFR-3%HGF
Cinobufacini injection%HLEC%Proliferation%Migration%Tube-like structure formation%VEGFR-3%HGF
背景与目的:华蟾素注射液是一种传统抗肿瘤中药制剂,目前药效机制尚不明确.本研究旨在探讨华蟾素注射液对人淋巴管内皮细胞(human lymphatic endothelial cells,HLEC)增殖、迁移和管状结构形成的影响.方法:通过绘制细胞生长曲线,观察华蟾素注射液对HLEC增殖的影响;通过细胞迁移实验观察华蟾素注射液对HLEC迁移的影响;通过基质胶实验观察华蟾素注射液对HLEC管状结构形成的影响;采用蛋白质印迹法(Western blot)观察华蟾素注射液对HLEC中VEGFR-3及HGF蛋白表达的影响.结果:随着华蟾素注射液药物浓度增加(0.105、0.21和0.42μg/mL),HLEC抑制率逐渐增高,迁移率分别为0.87±0.07、0.69±0.05、0.37±0.02,对照组为1±0.03;HLEC成管率为0.90±0.06、0.83±0.02、0.63±0.05,对照组为1±0.02, VEGFR-3/β-actin光密度比值为0.440±0.017、0.618±0.100、0.803±0.091,对照组为1.030±0.017;HGF/β-actin光密度比值为0.293±0.021、0.540±0.027、0.760±0.087,对照组为0.940±0.020(P<0.05).结论:华蟾素注射液能够显著抑制HLEC增殖、迁移及管状结构形成,并下调VEGFR-3和HGF蛋白的表达,对VFGFR-3信号转导通路的影响可能是抑制肿瘤淋巴道转移的机制之一.
揹景與目的:華蟾素註射液是一種傳統抗腫瘤中藥製劑,目前藥效機製尚不明確.本研究旨在探討華蟾素註射液對人淋巴管內皮細胞(human lymphatic endothelial cells,HLEC)增殖、遷移和管狀結構形成的影響.方法:通過繪製細胞生長麯線,觀察華蟾素註射液對HLEC增殖的影響;通過細胞遷移實驗觀察華蟾素註射液對HLEC遷移的影響;通過基質膠實驗觀察華蟾素註射液對HLEC管狀結構形成的影響;採用蛋白質印跡法(Western blot)觀察華蟾素註射液對HLEC中VEGFR-3及HGF蛋白錶達的影響.結果:隨著華蟾素註射液藥物濃度增加(0.105、0.21和0.42μg/mL),HLEC抑製率逐漸增高,遷移率分彆為0.87±0.07、0.69±0.05、0.37±0.02,對照組為1±0.03;HLEC成管率為0.90±0.06、0.83±0.02、0.63±0.05,對照組為1±0.02, VEGFR-3/β-actin光密度比值為0.440±0.017、0.618±0.100、0.803±0.091,對照組為1.030±0.017;HGF/β-actin光密度比值為0.293±0.021、0.540±0.027、0.760±0.087,對照組為0.940±0.020(P<0.05).結論:華蟾素註射液能夠顯著抑製HLEC增殖、遷移及管狀結構形成,併下調VEGFR-3和HGF蛋白的錶達,對VFGFR-3信號轉導通路的影響可能是抑製腫瘤淋巴道轉移的機製之一.
배경여목적:화섬소주사액시일충전통항종류중약제제,목전약효궤제상불명학.본연구지재탐토화섬소주사액대인림파관내피세포(human lymphatic endothelial cells,HLEC)증식、천이화관상결구형성적영향.방법:통과회제세포생장곡선,관찰화섬소주사액대HLEC증식적영향;통과세포천이실험관찰화섬소주사액대HLEC천이적영향;통과기질효실험관찰화섬소주사액대HLEC관상결구형성적영향;채용단백질인적법(Western blot)관찰화섬소주사액대HLEC중VEGFR-3급HGF단백표체적영향.결과:수착화섬소주사액약물농도증가(0.105、0.21화0.42μg/mL),HLEC억제솔축점증고,천이솔분별위0.87±0.07、0.69±0.05、0.37±0.02,대조조위1±0.03;HLEC성관솔위0.90±0.06、0.83±0.02、0.63±0.05,대조조위1±0.02, VEGFR-3/β-actin광밀도비치위0.440±0.017、0.618±0.100、0.803±0.091,대조조위1.030±0.017;HGF/β-actin광밀도비치위0.293±0.021、0.540±0.027、0.760±0.087,대조조위0.940±0.020(P<0.05).결론:화섬소주사액능구현저억제HLEC증식、천이급관상결구형성,병하조VEGFR-3화HGF단백적표체,대VFGFR-3신호전도통로적영향가능시억제종류림파도전이적궤제지일.
Background and purpose:The cinobufacini injection is a traditional antitumor drug. However, its mechanism is still unclear. The purpose of this study was to observe the effect of cinobufacini injection on proliferation, migration and tube-like structure formation of human lymphatic endothelial cells (HLEC). Methods:Cell growth curve was used to observe the effect of cinobufacini injection on the proliferation of HLEC;Migration assay was used to observe the effect of cinobufacini injection on the migration of HLEC;Matrigel assay was used to observe the effect of cinobufacini injection on the tube-like structure formation of HLEC;Western blot was used to analyze the expression of VEGFR-3 and HGF in HLEC under the action of cinobufacini injection. Results:With the increase of cinobufacini injection concentration (0.105, 0.21 and 0.42 μg/mL), HLEC inhibition rate gradually increased;Migration rates were 0.87±0.07, 0.69±0.05, and 0.37±0.02;and 1±0.03 in control group. HLEC into the tube rates were 0.90±0.06, 0.83±0.02, and 0.63±0.05;and 1±0.02 in control group. VEGFR-3/β-actin optical density ratios were 0.440±0.017, 0.618±0.100, and 0.803±0.091;and 1.030±0.017 in the control group. HGF/β-actin ratios of the optical density were 0.293±0.021, 0.540±0.027, and 0.760±0.087;and 0.940±0.020 in control group (P<0.05). Which showed that cinobufacini injection significantly inhibited HLEC proliferation (P<0.05), migration (P<0.05) and tube-like structure formation in dose dependent ways(P<0.05). Cinobufacini injection significantly descreased the expression of VEGFR-3 and HGF in HLEC in dose dependent ways(P<0.05). Conclusion:Cinobufacini injection significantly inhibits HLEC proliferation, migration and tube-like structure formation, and the down-regulation of VEGFR-3 and HGF may contribute to the inhibition of cinobufacini injection on HLEC.
