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目的:探讨裂果薯乙醇提取物对人肝癌裸鼠移植瘤生长与肿瘤血管生成的影响及其抗肿瘤的作用机制。方法:采用80%乙醇回流提取制备裂果薯块茎醇提物;建立人肝癌细胞SMMC-7721裸鼠移植瘤模型,成瘤BALB/c裸鼠随机分为模型组、索拉非尼组和裂果薯醇提物高、中、低剂量组;裂果薯高、中、低剂量组和索拉非尼组给药量分别为107,71,54,30 mg·kg-1·d-1,每日ig给药1次,连续给药21 d,模型组不给药,对比观察裂果薯醇提物对肿瘤生长的影响;免疫组化法测定裸鼠肿瘤中CD34,血管内皮生长因子(VEGF)的表达,观察裂果薯醇提物对肿瘤血管生成的影响。结果:与模型组相比,裂果薯醇提物高、中剂量组和索拉非尼组能够明显降低肿瘤瘤重和相对体积,其抑瘤率分别为47.71%,21.27%,51.75%;同时,裂果薯高剂量组、索拉非尼组能明显降低肿瘤微血管密度(MVD),(P<0.01),明显降低肿瘤组织中VEGF的表达(P<0.01);裂果薯中剂量组降低MVD(P<0.05)。结论:裂果薯醇提物可抑制SMMC-7721细胞裸鼠移植瘤和瘤组织中血管生长,其作用可能与下调VEGF的表达有关。
Objective: To investigate the effect of ethanol extract from split sweet potato on growth and tumor angiogenesis of human hepatocellular carcinoma in nude mice and its anti-tumor mechanism. Methods: Alcohol extract of tuber buds was prepared by 80% ethanol reflux extraction. The transplanted tumor model of human hepatocellular carcinoma cell line SMMC-7721 was established. BALB / c nude mice were randomly divided into model group, sorafenib group, Medium, low dose group, high dose group, low dose group and sorafenib group were 107, 71, 54 and 30 mg · kg-1 · d-1 daily ig administration once a day, continuous administration of 21 d, the model group is not administered, the contrast observation of the split sweet potato alcohol extract on tumor growth; immunohistochemistry in nude mice tumor CD34, vascular endothelial growth factor (VEGF) Expression and observation of the effects of the alcoholic extracts of Triticum chinense on tumor angiogenesis. Results: Compared with the model group, the tumor weight and relative volume of the ethanol extract of Triticum aestivum could significantly reduce the tumor weight and relative volume, and the antitumor rates were 47.71%, 21.27% and 51.75%, respectively; meanwhile, (P <0.01), and significantly decreased the expression of VEGF in tumor tissue (P <0.01). The medium-dose split-potato group reduced the MVD (MVD) P <0.05). CONCLUSION: Alcoholic extracts of Triticum chinense can inhibit the growth of xenografts and tumor tissues in nude mice SMMC-7721 cells, which may be related to the downregulation of VEGF expression.