人参-三七-川芎提取物对高糖高脂诱导血管内皮细胞衰老的影响

王雪; 修成奎; 杨静; 方靖漪; 雷燕

doi:10.13422/j.cnki.syfjx.20190125

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人参-三七-川芎提取物对高糖高脂诱导血管内皮细胞衰老的影响

药理 | 更新时间：2021-02-09

- 人参-三七-川芎提取物对高糖高脂诱导血管内皮细胞衰老的影响
- Interventional Effect and Mechanism of Extract of Ginseng Radix et Rhizoma, Notoginseng Radix et Rhizoma and Chuanxiong Rhizoma on Vascular Endothelial Cellular Senescence Induced by High Glucose and High Fat
- 中国实验方剂学杂志 2019年25卷第1期页码：124-129
- 作者机构：
  
  1.中国中医科学院　医学实验中心，北京　 100700
  2.广东药科大学　中医药研究院广东省代谢性疾病中西医结合研究中心，广州　 510006
- 作者简介：
  
  王雪，在读博士，从事中西医结合心血管病相关研究，E-mail：wx20087278@163.com
  雷燕，首席研究员，博士生导师，从事中西结合心血管方向研究，Tel：010-64089556，E-mail:13651217893@163.com
- 基金信息：
  
  国家自然科学基金面上项目(81673822);中国中医科学院自主选题(ZZ2017011)
- DOI：10.13422/j.cnki.syfjx.20190125
  中图分类号： R2-0;R22;R285.5
- 收稿日期：2018-07-09，
  
  网络出版日期：2018-10-17，
  
  纸质出版日期：2019-01-05
- 稿件说明：
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王雪, 修成奎, 杨静, 等. 人参-三七-川芎提取物对高糖高脂诱导血管内皮细胞衰老的影响[J]. 中国实验方剂学杂志, 2019,25(1):124-129.

Xue WANG, Cheng-kui XIU, Jing YANG, et al. Interventional Effect and Mechanism of Extract of Ginseng Radix et Rhizoma, Notoginseng Radix et Rhizoma and Chuanxiong Rhizoma on Vascular Endothelial Cellular Senescence Induced by High Glucose and High Fat[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(1): 124-129.
王雪, 修成奎, 杨静, 等. 人参-三七-川芎提取物对高糖高脂诱导血管内皮细胞衰老的影响[J]. 中国实验方剂学杂志, 2019,25(1):124-129. DOI： 10.13422/j.cnki.syfjx.20190125.

Xue WANG, Cheng-kui XIU, Jing YANG, et al. Interventional Effect and Mechanism of Extract of Ginseng Radix et Rhizoma, Notoginseng Radix et Rhizoma and Chuanxiong Rhizoma on Vascular Endothelial Cellular Senescence Induced by High Glucose and High Fat[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(1): 124-129. DOI： 10.13422/j.cnki.syfjx.20190125.

摘要

目的：

观察益气活血中药人参、三七、川芎提取物延缓高糖高脂诱导的血管内皮细胞衰老的分子生物学机制。

方法：

采用40 mmol·L

－1

葡萄糖和100 μmol·L

－1

棕榈酸钠造模，实验分为空白组、模型组和中药低、中、高剂量组（50，100，200 mg·L

－1

），干预48 h。采用细胞增殖与活性检测（CCK-8）检测细胞增殖能力；细胞衰老

-半乳糖苷酸（SA-gal）染色检测细胞衰老程度；蛋白免疫印迹法（Western blot）检测细胞p16，p21蛋白表达水平的变化；免疫荧光检测p-H2A.X（Ser139）表达，线粒体ROS（mtROS）产生和线粒体膜电位（MMP）改变。

结果：

与空白组比较，模型组细胞增殖能力及MMP水平降低（

0.01），SA-

-gal蓝染细胞数量，mtROS生成和p16，p21，p-H2A.X（Ser139）表达增加（

0.05，

0.01）；而与模型组比较，人参-三七-川芎提取物可提高细胞增殖能力和MMP水平（

0.01），减少SA-

-gal蓝染细胞数量和mtROS生成（

0.01），并能够降低p16，p21和p-H2A.X（Ser139）的表达水平（

0.05，

0.01）。

结论：

益气活血中药人参-三七-川芎提取物能够延缓高糖高脂引起的血管内皮细胞衰老，其机制可能与升高线粒体膜电位，减少ROS生成引起的DNA损伤累积有关。

Abstract

Objective:

To explore the mechanism of extract of Ginseng Radix et Rhizoma

Notoginseng Radix et Rhizoma and Chuanxiong Rhizoma in delaying the senescence of vascular endothelial cells induced by high glucose and high fat.

Method:

The 40 mmol·L

-1

glucose and 100 μmol·L

-1

palmitate were used to induce endothelial cell senescence. The experiment was divided into control group

model group and low

medium and high-dose traditional Chinese medicine groups (50

100

200 mg·L

-1

). The intervention lasted for 48 h. Cell proliferation was detected by cell counting kit-8(CCK-8); cell senescence was detected by senescence

-galactosidase staining; p16 and p21 protein expression levels were detected by Western blot; p-H2A.X(Ser139)expression

mitochondria ROS(mtROS) production and changes in mitochondrial membrane potential(MMP) were detected by immunofluorescence.

Result:

Compared with the control group

in model group

the cell proliferation ability and the number of SA-

-gal blue-stained cells decreased(

0.01)

while the mtROS production and the expressions of p16

p21 and p-H2A.X(Ser139)increased(

0.05

0.01). Compared with the model group

extract of Ginseng Radix et Rhizoma

Notoginseng Radix et Rhizoma and Chuanxiong Rhizoma can increase cell proliferation and MMP levels(

0.01)

and reduce the number of SA-

-gal blue-stained cells

the mtROS production

and expression levels of p16

p21 and p-H2A.X(Ser139)(

0.05

0.01).

Conclusion:

The above results suggest that extract of Ginseng Radix et Rhizoma

Notoginseng Radix et Rhizoma and Chuanxiong Rhizoma delay of endothelial cellular senescence induced by high glucose and high fat

and its mechanism may be related to increasing mitochondrial membrane potential and reducing DNA damage accumulation caused by ROS production.

关键词

Keywords

references

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