世界中医药
文章摘要
引用本文:吕靖1,谭烨2,赵志敏3,黄恺3,沈丽2,陶艳艳2,刘平2,刘成海2,3,4,5.扶正化瘀组分复方抑制血管新生的抗肝纤维化作用机制[J].世界中医药,2015,10(02):.  
扶正化瘀组分复方抑制血管新生的抗肝纤维化作用机制
Fuzheng Huayu components formula exerted anti-liver fibrosis through inhibiting angiogenesis
投稿时间:2014-12-26  
DOI:10.3969/j.issn.1673-7202.2015.02.009
中文关键词:  肝纤维化  血管新生  扶正化瘀组分复方
English Keywords:Liver fibrosis  Angiogenesis  Fuzheng Huayu Components formula
基金项目:国家自然科学基金项目(编号:81173405);上海市医学领军人才计划(编号:LJ10005);上海中医药大学预算内项目(编号:2014YSN40)
作者单位
吕靖1,谭烨2,赵志敏3,黄恺3,沈丽2,陶艳艳2,刘平2,刘成海2,3,4,5 1 上海中医药大学附属曙光医院·肝硬化科上海201203
2 上海中医药大学附属曙光医院·肝病研究所上海201203
3 上海市中医临床重点实验室上海201203
4 上海高校中医内科学E-研究院上海201203
5 肝肾疾病病证教育部重点实验室上海201203 
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中文摘要:
      目的:本研究旨在探讨扶正化瘀组分复方的抗肝纤维化作用及其作用机制。方法:采用DMN诱导小鼠肝纤维化模型,以扶正化瘀方为阳性对照。以天狼猩红染色和羟脯氨酸含量评估肝纤维化程度;肝脏微血管成像和CD31标记微血管密度评价肝脏血管新生;western blot法检测肝组织VEGF-R2表达;通过计数转基因斑马鱼功能性节间血管数和碱性磷酸酶活性验证药物对血管的影响。结果:扶正化瘀组分复方可显著改善纤维化小鼠血清肝功能(P<0.01):减少肝组织胶原沉积(P<0.01);减少肝脏微血管数量(P<0.01);下调VEGFR2蛋白表达(P<0.01);抑制斑马鱼碱性磷酸酶活性。结论:扶正化瘀组分复方具有抑制DMN诱导小鼠肝纤维化模型肝组织纤维化的作用,其作用机制可能与抑制血管新生有关。
English Summary:
      The purpose of this study is to investigate the mechanism of Fuzheng Huayu Components formula against Liver Fibrosis relating to Angiogenesis. Methods: Using DMN-induced liver fibrosis model in mice,Fuzheng Huayu formula as positive control. Liver fibrosis was estimated by Sirius red staining and hydroxyproline content assay. Liver angiogenesis was evaluated by liver tissue microvascular imaging analysis and MVD labeled by CD31. VEGF-R2 expression was observed by western blot. Zebrafish functional intersegmental vessels count and alkaline phosphatase activity was to investigate angiogenesis. Results: Fuzheng Huayu Components formula can alleviate liver function in DMN mice (P<0.01).Liver collagen deposition and hydroxyproline content were reduced significantly (P<0.01). The hepatic microvasculature reduced(P<0.01) with the VEGFR2 protein expression down regulated accordingly(P<0.01). It also inhibited alkaline phosphatase activity in zebrafish. Conclusion: Fuzheng Huayu Components formula inhibited liver fibrosis in DMN-treated mice. Its mechanism may be related to inhibit angiogenesis.
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