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作 者:姚子涵[1] 邱艳艳[1] 贺雪[1] 袁玉霞[1] 唐雪瑶 张祎稀 殷佩浩[1]
机构地区:[1]上海中医药大学附属普陀医院,上海200062
出 处:《上海中医药大学学报》2017年第1期54-56,62,共4页Academic Journal of Shanghai University of Traditional Chinese Medicine
基 金:国家自然科学基金资助项目(81473482;81603464);国家中医药管理局"十二五"中医药重点学科(中西医结合临床)建设项目;上海市科委医学引导类(中;西医)科技支撑项目(16411972600);上海中医药大学中西医结合高原学科面上项目
摘 要:目的:通过实验研究观察蟾毒灵对人结肠癌血管新生的作用。方法:CCK-8法检测不同浓度蟾毒灵对人脐静脉内皮细胞增殖的影响;构建裸鼠人结肠癌移植瘤模型,随机分为对照组(0.9%生理盐水)、蟾毒灵组(1.5 mg·kg^(^(-1))·d^(-1)),药物干预4周后,观察各组裸鼠移植瘤瘤体生长情况,Western blot检测瘤体组织中血管内皮生长因子A(VEGFA)的表达。结果:蟾毒灵在2.5~320.0 ng/ml的浓度区间内,其对人脐静脉内皮细胞的生长抑制率为1.67%~95.40%,IC50为20.86 ng/ml,呈剂量依赖性。蟾毒灵组裸鼠移植瘤瘤体明显小于对照组(P<0.01),蟾毒灵组瘤体中VEGFA蛋白的表达明显低于对照组(P<0.05)。结论:蟾毒灵可抑制血管内皮细胞增殖,抑制裸鼠人结肠癌移植瘤瘤体的生长,其机制可能与下调VEGFA蛋白的表达有关。Objective: To investigate the effects of bufalin on human colorectal cancer angiogenesis. Methods: The effects of bufalin at different concentration on proliferation of human umbilical vein endothelial cells were detected by CCK-8 method. Transplanted tumor model of human colorectal cancer was established in nude mice, and then the mice were randomly divided into the control group which treated with normal saline and the bufalin group which treated with bufalin at the dose of 1.5 mg/kg a day. After drug intervention for 4 weeks, the growth of transplanted tumor in nude mice was observed, the expression of vascular endothelial growth factor A (VEGFA) in tumor tissues was detected by Western blot. Results: In the concentration range of 2.5-320.0 ng/ml, the growth inhibition rate of bufalin on human umbilical vein endothelial cells was 1.67% -95.40% ,which showed in a dose-dependent manner, IC50 was 20.86 ng/ml. The transplanted tumor in nude mice of the bufalin group was significantly smaller than that of the control group ( P 〈 0. 01 ). The protein expression of VEGFA in tumor tissues of the bufalin group was significantly lower than that of the control group( P 〈 0.05 ). Conclusion : Bufalin could inhibit the proliferation of vascular endothelial cells and the tumor growth in nude mice transplanted with human colorectal cancer. Its mechanism may be related to down-regulating the protein expression of VEGFA.
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