桂枝茯苓丸抑制大鼠子宫内膜异位症血管生成的作用及机制

万贵平; 张真真; 汤伟伟; 桂涛; 朱利; 马小平; 钱如云; 胡春萍; 曹鹏

doi:10.11653/syfj2014010161

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桂枝茯苓丸抑制大鼠子宫内膜异位症血管生成的作用及机制

更新时间：2024-01-04

- 桂枝茯苓丸抑制大鼠子宫内膜异位症血管生成的作用及机制
- Anti-angiogenesis Effects and Mechanism of Guizhi Fuling Wan on Endometriosis in a Rat Model
- 中国实验方剂学杂志 2014年20卷第1期页码：161-165
- 作者机构：
- 作者简介：
- 基金信息：
  
  江苏省中医药局科技项目（LZ11057）;江苏省高校优势学科建设工程一期项目（YS2012ZYX315）;江苏省中医药研究院引进人才科研启动基金（RC1107）
- DOI：10.11653/syfj2014010161
  中图分类号：
- 纸质出版日期：2014
- 稿件说明：
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万贵平, 张真真, 汤伟伟, 等. 桂枝茯苓丸抑制大鼠子宫内膜异位症血管生成的作用及机制[J]. 中国实验方剂学杂志, 2014,20(1):161-165.

WAN Gui-ping, ZHANG Zhen-zhen, TANG Wei-wei, et al. Anti-angiogenesis Effects and Mechanism of Guizhi Fuling Wan on Endometriosis in a Rat Model[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(1): 161-165.
万贵平, 张真真, 汤伟伟, 等. 桂枝茯苓丸抑制大鼠子宫内膜异位症血管生成的作用及机制[J]. 中国实验方剂学杂志, 2014,20(1):161-165. DOI： 10.11653/syfj2014010161.

WAN Gui-ping, ZHANG Zhen-zhen, TANG Wei-wei, et al. Anti-angiogenesis Effects and Mechanism of Guizhi Fuling Wan on Endometriosis in a Rat Model[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(1): 161-165. DOI： 10.11653/syfj2014010161.

摘要

目的：探讨桂枝茯苓丸抑制大鼠子宫内膜异位症血管生成的作用及机制。方法：采用自体移植法建立大鼠子宫内膜异位症模型，分为模型对照组（阴性对照）、桂枝茯苓丸低、高剂量组（4.13，8.26 g·kg-1）、孕三烯酮组（阳性对照，0.23 g·kg-1）。另设假手术对照组。连续给药28 d后处死大鼠，免疫组化法检测异位内膜中的增殖细胞核抗原（PCNA）和血小板-内皮细胞黏附分子（CD31）的表达，酶联免疫吸附测定（ELISA）法检测腹腔液中血管内皮生长因子（VEGF）的水平，RT-qPCR检测异位内膜中VEGF和缺氧诱导因子-1α（HIF-1α）的表达。结果：桂枝茯苓丸显著抑制异位内膜中PCNA，CD31的表达，降低腹腔液中VEGF的水平（P<0.05）以及异位病灶中VEGF、缺氧诱导因子-1α（HIF-1α）的mRNA表达水平（P<0.01）。结论：桂枝茯苓丸显著抑制大鼠子宫内膜异位症的血管生成作用，其作用机制与抑制VEGF和HIF-1α的表达有关。

Abstract

Objective: To study the effects and mechanism of Guizhi Fuling Wan on inhibiting angiogenesis in a rat model of endometriosis. Method: Rat endometriosis model was induced by autologous transplantation. The rats with endometriosis were divided into control group (negative control)

low dose Guizhi Fuling Wan group (4.13 g·kg-1)

high-dose Guizhi Fuling Wan group (8.26 g·kg-1) and gestrinone group (positive control

0.23 g·kg-1). There was also a sham-operated group. After treatment for 28 days

the rats were killed by cervical dislocation. The expression of prolifarating cell nuclear antigen(PCNA) and CD31 in ectopic endometrium was assessed by immunohistochemistry. The level of vascular endothelial growth factor(VEGF) in peritoneal fluid (PF) was determined by ELISA. The mRNA expression of VEGF and hypoxia inducible fuctor-1 HIF-1α in ectopic endometrium was evaluated by real-time PCR. Result: After treatment

Guizhi Fuling Wan could suppresse the expression of PCNA and CD31 in ectopic endometrium

decline concentration of VEGF in PF (P<0.05)

and reduce mRNA expression of VEGF and HIF-1α in ectopic endometrium (P<0.01). Conclusion: Guizhi Fuling Wan significantly suppress angiogenesis in a rat endometriosis model

and the mechanism may be related to the inhibition expression of VEGF and HIF-1α.

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