Hepatotoxic Material Basis of Polygoni Multiflori Radix with Zebrafish Model

Yun-yun QUAN; Yi-meng ZHOU; Mei-chen LIU; Yun-xia LI

doi:10.13422/j.cnki.syfjx.20190523

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Hepatotoxic Material Basis of Polygoni Multiflori Radix with Zebrafish Model

Pharmacology | 更新时间：2021-02-09

- Hepatotoxic Material Basis of Polygoni Multiflori Radix with Zebrafish Model
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 25, Issue 6, Pages: 52-57(2019)
- 作者机构：
  
  成都中医药大学　药学院，教育部中药材标准化重点实验室，中药资源系统研究与开发利用省部共建国家重点实验室培育基地，成都　 611137
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20190523
  CLC： R22;R242;R2-031;R285.5;R273
- Received：28 August 2018，
  
  Published Online：2018-20-11，
  
  Published：20 March 2019
- 稿件说明：
移动端阅览
Yun-yun QUAN, Yi-meng ZHOU, Mei-chen LIU, et al. Hepatotoxic Material Basis of Polygoni Multiflori Radix with Zebrafish Model[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(6): 52-57.
DOI：

Yun-yun QUAN, Yi-meng ZHOU, Mei-chen LIU, et al. Hepatotoxic Material Basis of Polygoni Multiflori Radix with Zebrafish Model[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(6): 52-57. DOI： 10.13422/j.cnki.syfjx.20190523.

摘要

目的：

用斑马鱼模型探索何首乌肝毒性物质基础，为何首乌肝毒性作用机制研究提供一定的理论依据。

方法：

将对实验前期所筛选出来的大黄素、大黄酸、芦荟大黄素、大黄素-1-

-葡萄糖苷、大黄素甲醚-8-

-葡萄糖苷、芦荟大黄素-8-

-葡萄糖苷（质量浓度分别为0.000 73，0.002 22，0.015 05，0.002 36，0.198 95，0.072 73 g·L

－1

）这6种何首乌中的化学成分，继续使用肝脏荧光转基因斑马鱼为动物模型，对受精后72 h的幼鱼连续给药3 d。分别测定给药后1，2，3 d的斑马鱼体内丙氨酸氨基转移酶（ALT），天门冬氨酸氨基转移酶（AST），谷胱甘肽（GSH）的活力和总胆红素（TBIL）的含量，分别对其进行切片分析，观察斑马鱼肝脏组织病理学改变。

结果：

大黄素、大黄酸、大黄素-1-

-葡萄糖苷、大黄素甲醚-8-

-葡萄糖苷对斑马鱼体内ALT，AST，GSH的活力和TBIL的含量无明显影响，其斑马鱼肝组织显示正常；芦荟大黄素能显著降低斑马鱼体内ALT，AST，GSH的活力(

0.01)，显著升高TBIL含量(

0.01)；芦荟大黄素-8-

-葡萄糖苷能显著降低斑马鱼体内ALT，GSH的活力(

0.01)，明显升高TBIL含量(

0.05，

0.01)，对斑马鱼体内AST的活力无明显影响，同时此二者的斑马鱼肝组织均出现大片片状坏死，肝组织细胞发生明显形态改变，肝细胞排列不规则等。

结论：

何首乌中的芦荟大黄素和芦荟大黄素-8-

-葡萄糖苷可对斑马鱼肝脏产生毒性作用，提示芦荟大黄素和芦荟大黄素-8-

-葡萄糖苷可能是何首乌的肝毒性物质基础。

Abstract

Objective:

To explore the hepatotoxic material basis of Polygoni Multiflori Radix with zebrafish model

in order to provide a theoretical basis for the study on the mechanism of Polygoni Multiflori Radix hepatotoxicity.

Method:

Emodin

rhein

aloe emodin

emodin-1-

-glucoside

physcion-8-

-glucoside and aloe emodin-8-

-glucoside for three days (at the concentrations of 0.000 73

0.002 22

0.015 05

0.002 36

0.198 95

0.072 73 g·L

-1

) selected from the early stage of the experiment were continuously administered to zebrafish fertilized for 72 hours to establish the liver fluorescence transgenic larvae animal model. The activities of alanine aminotransferase (ALT)

aspartate aminotransferase (AST)

glutathione (GSH) and total bilirubin (TBIL) in zebrafish at 1

3 day after administration were measured respectively

and the pathological changes of zebrafish liver tissue were analyzed.

Result:

Emodin

rhein

emodin-1-

-glucoside and physcion-8-

-glucoside had no significant effect on the activities of ALT

AST

GSH and content of TBIL (

0.01) in zebrafish

and the liver tissue of zebrafish was normal; aloe-emodin could significantly reduce the activities of ALT

AST

GSH (

0.01)

whereas increase the content of TBIL in zebrafish; aloe-emodin-8-

-glucoside could significantly reduce the activities of ALT

GSH

whereas increased the content of TBIL (

0.05

0.01) in zebrafish

with no significant effect on the activity of AST

then both groups showed large flaky necrosis in zebrafish liver tissue

obvious morphologic changes in liver tissue cells

and irregular arrangement of hepatocytes.

Conclusion:

Aloe-emodin and aloe-emodin-8-

-glucoside in Polygoni Multiflori Radix have a toxic effect on zebrafish liver

suggesting that aloe-emodin and aloe-emodin-8-

-glucoside might be the hepatotoxic material basis of Polygoni Multiflori Radix.

关键词

Keywords

references

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Related Institution

Institute of Chinese Materia Medica，China Academy of Chinese Medical Sciences

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Key Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases of Xiangyang City， Xiangyang No.1 People's Hospital， Hubei University of Medicine， Xiangyang

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