黄芪甲苷对BALB/C小鼠肝癌H22腹水瘤抑制作用及机制

中国药物警戒 ›› 2016, Vol. 13 ›› Issue (3): 138-142.

黄芪甲苷对BALB/C小鼠肝癌H22腹水瘤抑制作用及机制

武建毅,沈清,金赟洁,姚晓祥,朱纪华,朱麟玉,黄晓东

上海市普陀区人民医院,上海 200060

收稿日期:2016-02-18 修回日期:2016-04-12 出版日期:2016-03-20 发布日期:2016-04-12
通讯作者: 黄晓东,男,副主任医师,呼吸道/消化道恶性肿瘤。 E-mail:huangxiaodong@sina.com
作者简介:武建毅,男,主治医师,硕士,肿瘤生物治疗。
基金资助:
江苏大学医学临床科技发展基金（JLY20140100）。

Inhibition and Mechanism of Astragaloside Ⅳ on H22 Ascites in BALB/C Mice

WU Jian-yi, SHEN Qing, JIN Yun-jie, YAO Xiao-xiang, ZHU Ji-hua, ZHU Lin-yu, HUANG Xiao-dong

Department of Oncology, Putuo District People’s Hospital of Shanghai, Shanghai 200060, China

Received:2016-02-18 Revised:2016-04-12 Online:2016-03-20 Published:2016-04-12

摘要/Abstract

摘要： 目的探讨黄芪甲苷对BALB/C小鼠肝癌H22腹水瘤的抑制作用及机制。方法 BALB/C小鼠100只,腹腔注射 H22 细胞建立小鼠肝癌H22腹水瘤模型后,随机分为阴性对照组（0.9% NS）、阳性对照组（0.5 mg·kg-1顺铂）、黄芪甲苷低（0.3 mg·kg-1）、中（1.0 mg·kg-1）、高（3.0 mg·kg-1）剂量组,每组20只,每日1次,连续给药14 d,末次给药24 h后处死小鼠,计算腹水量、瘤细胞抑制率及腹膜瘤最大结节直径, ELISA检测VEGF的含量,免疫组化检测 VEGF、MMP-2、MMP-9、AQP-1和CD31蛋白的表达。结果黄芪甲苷组腹水量、瘤细胞存活率以及最大结节直径均降低（P<0.05）; VEGF含量明显减少,与阴性对照组比较有显著差异（P<0.001）, VEGF、MMP-2、MMP-9、AQP-1和CD31蛋白的表达降低。结论黄芪甲苷通过影响血管生成、抑制转移相关基因和水通道蛋白的表达抑制H22腹水瘤肝癌。

关键词: 黄芪甲苷, H22腹水瘤, BALB/C小鼠, 抑制作用, 机制

Abstract: Objective To investigate the inhibition of astragaloside Ⅳ(AsⅣ) on H22 ascites in BALB/C mice and its mechanism. Methods H22 ascites mouse model was established by i.p. injecting 100 BALB/C mice with H22 cells. Mice were then divided randomly into 5 groups: negative control (0.9 % normal saline), positive control (DDP 0.5 mg·kg-1), low AsⅣ dose (0.3 mg·kg-1),intermediate AsⅣ dose (1.0 mg·kg-1) and high AsⅣ dose (3.0 mg·kg-1), 20 of each group, once a day for 14 days. 24 hours after the end of the treatment, mice of each group were executed, calculated the volume of ascites,cell-inhibition rate and the diameter of largest nodule . The content of VEGF in ascites was detected by ELISA, the protein expression was made by immunohistochemical detection of VEGF, MMP-2, MMP-9, AQP-1 and CD31. Results The volume of ascites, largest nodule diameter, tumor cell viability and the content of VEGF were decreased, compared with negative group, the difference was statistically significant (P<0.05). Also the protein expression of VEGF, MMP-2, MMP-9, AQP-1 and CD31 were decreased, compared with negative group. Conclusion H22 ascites in BALB/C mice were inhibited by astragaloside Ⅳ(AsⅣ) through the angiogenesis, inhibiting metastasis associated genes and the expression of aquaporin(AQPs).

Key words: astragaloside Ⅳ, H22 ascites, BALB/C mice, inhibition, mechanism

中图分类号:

R965
R285.5

武建毅,沈清,金赟洁,姚晓祥,朱纪华,朱麟玉,黄晓东. 黄芪甲苷对BALB/C小鼠肝癌H22腹水瘤抑制作用及机制[J]. 中国药物警戒, 2016, 13(3): 138-142.

WU Jian-yi, SHEN Qing, JIN Yun-jie, YAO Xiao-xiang, ZHU Ji-hua, ZHU Lin-yu, HUANG Xiao-dong. Inhibition and Mechanism of Astragaloside Ⅳ on H22 Ascites in BALB/C Mice[J]. Chinese Journal of Pharmacovigilance, 2016, 13(3): 138-142.

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