地锦草调控NF-B/VEGF信号通路抑制肿瘤血管生成的机制

胡建新; 席晓甜; 王晓敏; 邹志坚

doi:10.13422/j.cnki.syfjx.20182027

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地锦草调控NF-B/VEGF信号通路抑制肿瘤血管生成的机制

药理 | 更新时间：2024-09-23

- 地锦草调控NF-B/VEGF信号通路抑制肿瘤血管生成的机制
- Mechanism of in Regulating Tumor Angiogenesis by NF-B/VEGF Signal Pathway
- 中国实验方剂学杂志 2018年24卷第23期页码：165-170
- 作者机构：
- 作者简介：
- 基金信息：
  
  江西省教育厅科学技术研究项目（14103）
- DOI：10.13422/j.cnki.syfjx.20182027
  中图分类号： R285.5
- 纸质出版日期：2018
- 稿件说明：
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胡建新, 席晓甜, 王晓敏, 等. 地锦草调控NF-B/VEGF信号通路抑制肿瘤血管生成的机制[J]. 中国实验方剂学杂志, 2018,24(23):165-170.

HU Jian-xin, XI Xiao-tian, WANG Xiao-min, et al. Mechanism of in Regulating Tumor Angiogenesis by NF-B/VEGF Signal Pathway[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(23): 165-170.
胡建新, 席晓甜, 王晓敏, 等. 地锦草调控NF-B/VEGF信号通路抑制肿瘤血管生成的机制[J]. 中国实验方剂学杂志, 2018,24(23):165-170. DOI： 10.13422/j.cnki.syfjx.20182027.

HU Jian-xin, XI Xiao-tian, WANG Xiao-min, et al. Mechanism of in Regulating Tumor Angiogenesis by NF-B/VEGF Signal Pathway[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(23): 165-170. DOI： 10.13422/j.cnki.syfjx.20182027.

摘要

目的：通过观察地锦草对H22肝癌小鼠核转录因子-κB/血管内皮生长因子（nuclear factor kappa-B/vascular endothelial growth factor，NF-κB/VEGF）信号通路相关蛋白的影响，探讨地锦草抑制肿瘤血管生成的机制。方法：昆明种小鼠皮下接种肝癌H22细胞建立H22肝癌小鼠模型，随机分为模型组，环磷酰胺组，地锦草组高、中、低剂量组。地锦草低、中、高剂量组分别灌胃（ig）给药1.13，2.25，4.50 g·kg-1，环磷酰胺组腹腔注射（ip）给药50 mg·kg-1，模型组和环磷酰胺组灌服相同体积的蒸馏水，14 d后处死小鼠，测量肿瘤质量和小鼠体质量，计算抑瘤率；免疫组织化学检测微血管密度标记物血小板-内皮细胞黏附分子31（platelet endothelial cell adhesion molecule-31，CD31），聚合酶链反应检测肿瘤组织NF-κB，肿瘤坏死因子（TNF）-α，VEGF mRNA表达，免疫组化检测NF-κB，TNF-α，VEGF蛋白表达。结果：与模型组比较，给予地锦草后，H22肝癌小鼠瘤重减轻（P<0.01），地锦草高剂量组抑瘤率升高，高达59.1%（P<0.01）；肿瘤组织CD31表达明显下降（P<0.01）；肿瘤组织NF-κB，TNF-α，VEGF mRNA和蛋白表达均下降（P<0.01）。结论：地锦草对H22肝癌小鼠肿瘤的抑制作用可能是通过减少肿瘤新生血管的生成，与减弱肿瘤组织的炎性因子表达有关。

Abstract

Objective:To observe the mechanism of Humifuse euphorbia on tumor angiogenesis in H22 liver cancer mice by regulating signal pathway of nuclear factor kappa-B/vascular endothelial growth factor (NF-κB/VEGF). Method:The models of SPF grade Kunming mice with H22 liver cancer were established through armpit injection. The animals with successful modeling were randomly divided into five groups:model control group

cyclophosphamide group (ip

50 mg·kg-1)

high-dose group (ig

4.50 g·kg-1)

middle-dose group (ig

2.25 g·kg-1) and low-dose group (ig

1.13 g·kg-1)

with 10 mice in each group. Their weights and tumor weights were measured after the 14-day drug administration. Index of tumor was calculated. Tumor micro-vessel density

which was marked as platelet endothelial cell adhesion molecule-31

was detected by immunohistochemitry. Tumor tissue NF-κB

VEGF

tumor necrosis factor-α(TNF-α)mRNA expressions were detected by polymerase chain reaction and protein expression by immunohistochemitry. Result:Compared with model group

H. euphorbia could significantly reduce tumor weigh (P<0.01). High-dose group showed an inhibition rate of 59.1% for H22 liver cancer in mice. CD31 expression of the high-dose group was significantly lower than that of the model group

while the expressions of NF-κB

TNF-α

VEGF mRNA and protein in tumor tissue were significantly decreased (P<0.01). Conclusion:H. euphorbia can inhibit the growth of H22 liver cancer mice

and its mechanism is probably related to the inhibition of the growth of tumor angiogenesis

which may activate NF-κB/VEGF signaling pathway.

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