黄芪甲苷对“铁超载”所致小鼠肝损伤的保护作用

叶枝红; 谢海纳; 钱知知; 叶晶; 姜文静; 刘霖; 谢东浩; 张良

doi:10.13422/j.cnki.syfjx.20180735

您当前的位置：

首页 >

文章列表页 >

黄芪甲苷对“铁超载”所致小鼠肝损伤的保护作用

药理 | 更新时间：2024-01-04

- 黄芪甲苷对“铁超载”所致小鼠肝损伤的保护作用
- Protective Effect of Astragaloside on Liver Injury Induced by Iron Overload in Mice
- 中国实验方剂学杂志 2018年24卷第8期页码：116-121
- 作者机构：
- 作者简介：
- 基金信息：
  
  上海市徐汇区医学科研项目（SHXH201310）
- DOI：10.13422/j.cnki.syfjx.20180735
  中图分类号： R285.5
- 纸质出版日期：2018
- 稿件说明：
移动端阅览
叶枝红, 谢海纳, 钱知知, 等. 黄芪甲苷对“铁超载”所致小鼠肝损伤的保护作用[J]. 中国实验方剂学杂志, 2018,24(8):116-121.

YE Zhi-hong, XIE Hai-na, QIAN Zhi-zhi, et al. Protective Effect of Astragaloside on Liver Injury Induced by Iron Overload in Mice[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(8): 116-121.
叶枝红, 谢海纳, 钱知知, 等. 黄芪甲苷对“铁超载”所致小鼠肝损伤的保护作用[J]. 中国实验方剂学杂志, 2018,24(8):116-121. DOI： 10.13422/j.cnki.syfjx.20180735.

YE Zhi-hong, XIE Hai-na, QIAN Zhi-zhi, et al. Protective Effect of Astragaloside on Liver Injury Induced by Iron Overload in Mice[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(8): 116-121. DOI： 10.13422/j.cnki.syfjx.20180735.

摘要

目的：研究黄芪甲苷对铁超载造成肝损伤保护的作用机制。方法：小鼠按体质量随机分为空白组，模型组、黄芪甲苷（As）低、中、高剂量组。连续给药45 d，取血清，检测血清Fe，总铁结合力（total iron binding capacity，TIBC），丙氨酸氨基转移酶（glutamic-pyruvic transaminase，ALT），天门冬氨酸氨基转移酶（glutamic oxalacetic transaminase，AST），总胆红素（total bilirubin，T-BIL），丙二醛（malondialdehyde，MDA），谷胱甘肽（glutathione，GSH）水平；用苏木素-伊红（HE）染色观察肝脏病理组织学变化；用免疫组化法分析肝脏组织蛋白硝化的表达变化；用原位末端转移酶标记技术（TUNEL）染色法观察肝细胞凋亡的变化。结果：与空白组比较，模型组小鼠血清中血清Fe，ALT，AST，MDA，肝中铁和T-BIL含量显著增加（P<0.01），而TIBC和GSH含量显著降低（P<0.05，P<0.01）；与模型组比较，黄芪甲苷组小鼠血清中血清Fe，ALT，AST，MDA水平，及肝中Fe和T-BIL含量显著降低（P<0.05，P<0.01），肝中TIBC和GSH含量显著增高（P<0.05，P<0.01）；HE结果显示，与空白组比较，铁超载组可见肝细胞水样变性、肝细胞脂肪变性和炎症细胞浸润等；不同浓度黄芪甲苷组的上述病理改变得以改善；免疫组化结果发现，与空白组比较，铁超载组血管周围细胞浆中3-硝基酪氨酸（3-NT）显著增加，而黄芪甲苷组血管膜周围的3-硝基酪氨酸则显著减少；TUNEL染色发现与空白组比较，模型组肝细胞凋亡显著增多；与模型组比较，黄芪甲苷组肝细胞凋亡显著减少。结论：黄芪甲苷对铁超载造成的肝损伤具有保护作用。

Abstract

Objective: To investigate the protective role of astragaloside (As) in the liver injury caused by iron overload. Method: The mice were randomly divided into blank control group

model group

as low-dose group

as middle-dose group and as high-dose group according to their weight. Mice were intraperitoneally injected with As once daily for 45 d. Then their serum was taken to determine the content of serum iron

total iron binding capacity (TIBC)

alanine aminotransferase (ALT)

aspartate aminotransferase (AST)

total bilirubin (T-BIL)

malondialdehyde (MDA)

and glutathione (GSH); pathological changes in liver tissues were examined by hematoxylin-eosin (HE) staining; the expression changes of protein nitration in liver tissues were detected by immunohistochemical staining; and the changes of the liver apoptosis were observed by TdT-mediated dUTP nick end labeling (TUNEL) staining. Result: As compared with the blank group

the levels of serum Fe

MDA

ALT

and AST in serum as well as Fe and T-BIL in liver were increased in the model group (P<0.01)

while the levels of GSH and TIBC were decreased significantly (P<0.05

P<0.01). However

as compared with the model group

the levels of serum Fe

MDA

ALT and AST in serum as well as Fe and T-BIL levels in liver were significantly decreased in the As groups (P<0.05

P<0.05)

while the levels of GSH and TIBC in liver were significantly decreased (P<0.05

P<0.01). HE results showed that as compared with blank group

hepatocyte hydropic degeneration

hepatocyte fatty degeneration and inflammatory cell infiltration were present in iron overload group; but these pathological damages were improved in different dose As groups. Immunohistochemical results showed that as compared with the blank group

the 3-nitrotyrosine (3-NT) level in the perivascular plasma was increased significantly in the iron overload group

but was significantly reduced in the As groups. TUNEL staining results showed that as compared with the blank group

hepatocyte apoptosis was significantly increased in model group; as compared with the model group

the hepatocyte apoptosis was significantly reduced in As groups. Conclusion: As could attenuate the liver injury induced by iron overload.

关键词

Keywords

references

浏览量

下载量

CSCD

文章被引用时，请邮件提醒。

提交

工具集

关联资源

犀角地黄汤干预PKM2介导的一碳代谢途径调控脓毒症炎症反应的机制

线粒体质量控制调控肌少症发病机制及其中医药干预的研究进展

药食同源保肝中药的抗炎抗氧化作用

当归芍药散加味调控JNK/p38 MAPK通路改善痤疮炎症和凋亡的机制

子宫内膜异位症程序性细胞死亡和中医药干预作用研究进展