现代肿瘤医学
現代腫瘤醫學
현대종류의학
Journal of Modern Oncology
2015年
19期
2712-2715
,共4页
姜黄素%CaSki 细胞株%裸鼠%移植瘤%VEGF - C%VEGFR - 3
薑黃素%CaSki 細胞株%裸鼠%移植瘤%VEGF - C%VEGFR - 3
강황소%CaSki 세포주%라서%이식류%VEGF - C%VEGFR - 3
curcumin%CaSki cell line%nude mice%transplantable tumor%VEGF - C%VEGFR - 3
目的:探讨姜黄素对人宫颈癌裸鼠皮下移植瘤淋巴管生成及淋巴道转移的影响。方法:取对数生长期 CaSki 细胞接种于裸鼠右腋窝皮下,建立人宫颈癌裸鼠皮下移植瘤模型,免疫组化方法检测移植瘤组织中VEGF - C 和 VEGFR -3蛋白表达情况。结果:免疫组化显示姜黄素处理组的肿瘤组织 VEGF - C、VEGFR -3蛋白表达水平较阴性对照组降低(P <0.05)。可见姜黄素能下调肿瘤细胞中 VEGF - C 和 VEGFR -3蛋白的表达。结论:姜黄素具有抗宫颈癌淋巴管生成的作用,对宫颈癌淋巴道转移具有抑制作用,其主要机制与抑制 VEGF - C 和 VEGFR -3蛋白的表达有关。
目的:探討薑黃素對人宮頸癌裸鼠皮下移植瘤淋巴管生成及淋巴道轉移的影響。方法:取對數生長期 CaSki 細胞接種于裸鼠右腋窩皮下,建立人宮頸癌裸鼠皮下移植瘤模型,免疫組化方法檢測移植瘤組織中VEGF - C 和 VEGFR -3蛋白錶達情況。結果:免疫組化顯示薑黃素處理組的腫瘤組織 VEGF - C、VEGFR -3蛋白錶達水平較陰性對照組降低(P <0.05)。可見薑黃素能下調腫瘤細胞中 VEGF - C 和 VEGFR -3蛋白的錶達。結論:薑黃素具有抗宮頸癌淋巴管生成的作用,對宮頸癌淋巴道轉移具有抑製作用,其主要機製與抑製 VEGF - C 和 VEGFR -3蛋白的錶達有關。
목적:탐토강황소대인궁경암라서피하이식류림파관생성급림파도전이적영향。방법:취대수생장기 CaSki 세포접충우라서우액와피하,건립인궁경암라서피하이식류모형,면역조화방법검측이식류조직중VEGF - C 화 VEGFR -3단백표체정황。결과:면역조화현시강황소처리조적종류조직 VEGF - C、VEGFR -3단백표체수평교음성대조조강저(P <0.05)。가견강황소능하조종류세포중 VEGF - C 화 VEGFR -3단백적표체。결론:강황소구유항궁경암림파관생성적작용,대궁경암림파도전이구유억제작용,기주요궤제여억제 VEGF - C 화 VEGFR -3단백적표체유관。
Objective:To study the effects of curcumin on lymphangiogenesis and lymphatic metastasis of human cervical cancer subcutaneous xenograft in nude mice tube. Methods:To take the logarithmic growth phase of CaSki cells and inoculate them in nude mice right axillary subcutaneous,establish the model of human cervical carcinoma subcutaneous xenograft in nude mice and test VEGF - C and VEGFR - 3 protein in transplanted tumor by immunohis-tochemical method. Results:Immunohistochemical method showed that compared with the control group,expressions of VEGF - C and VEGFR - 3 in transplanted tumors were downregulated in curcumin groups. Curcumin can cut down the expression of VEGF - C and VEGFR - 3 protein in tumor cells. Conclusion:Curcumin has a significant anti -lymphangiogenesis activity. Curcumin has an inhibitory effect on the cervical lymph node metastasis,which may be re-lated with the inhibition expression of VEGF - C and VEGFR - 3.