Protective effect of mdivi-1 on heart of mice after acute myocardial ischemia

Qinghui LI; Yue WU; Lei KUANG; Tao LI

doi:10.16016/j.1000-5404.202102056

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Protective effect of mdivi-1 on heart of mice after acute myocardial ischemia

Basic Medicine | 更新时间：2026-01-09

- Protective effect of mdivi-1 on heart of mice after acute myocardial ischemia
- Journal of Third Military Medical University Vol. 43, Issue 14, Pages: 1326-1331(2021)
- 作者机构：
  
  400042 重庆，陆军特色医学中心野战外科研究部战伤休克与输血研究室，创伤、烧伤与复合伤国家重点实验室
- 作者简介：
- 基金信息：
  
  the Key Program of National Natural Science Foundation of China(81730059)
- DOI：10.16016/j.1000-5404.202102056
  CLC： R-332;R542.2;R977.6
- Received：08 February 2021，
  
  Revised：2021-04-12，
  
  Published：30 July 2021
- 稿件说明：
移动端阅览
Qinghui LI, Yue WU, Lei KUANG, et al. Protective effect of mdivi-1 on heart of mice after acute myocardial ischemia[J]. Journal of Third Military Medical University, 2021, 43(14): 1326-1331.
DOI：

Qinghui LI, Yue WU, Lei KUANG, et al. Protective effect of mdivi-1 on heart of mice after acute myocardial ischemia[J]. Journal of Third Military Medical University, 2021, 43(14): 1326-1331. DOI： 10.16016/j.1000-5404.202102056.

摘要

目的

观察线粒体分裂抑制剂mdivi-1对缺血小鼠心肌的保护作用。

方法

采用结扎心脏左前降支制作小鼠急性心肌缺血模型，将140只C57小鼠按随机数表分成4组，每组35只: 假手术组(只穿线不结扎)，假手术+mdivi-1组(穿线不结扎同时尾静脉注射mdivi-1)，缺血组(结扎心脏左前降支制作急性心肌缺血模型)，mdivi-1组(结扎心脏左前降支并尾静脉注射mdivi-1)。通过测定SOD、MDA、ATP、ROS、心肌损伤标志物并对心肌及细胞线粒体进行形态学观察，研究mdivi-1对心肌缺血小鼠心脏的保护作用。

结果

缺血后小鼠心肌结构显著受损且线粒体碎片化程度增高，排列紊乱，线粒体功能显著受损，表现为线粒体分裂抑制剂mdivi-1能显著减轻心肌线粒体结构及功能损伤，缺血心肌细胞周围损伤带缩窄、心肌ATP(1.587±0.227)μmol/mg和SOD(0.401±0.138)U/mg含量显著上升(

0.05)，ROS(4 276.0±687.5)荧光强度/mg和MDA(3.538±1.110)μmol/mg含量显著下降(

0.05)，降低心肌氧化损伤、心肌损伤标志物水平，保护心肌功能，显著延长模型小鼠存活时间，提高存活率。

结论

线粒体分裂抑制剂mdivi-1对心肌缺血小鼠心脏有保护作用。

Abstract

Objective

To observe the protective effect of mdivi-1

a mitochondrial fission inhibitor

on mice after myocardial ischemia.

Methods

A total of 140 C57 mice were randomly divided into 4 groups (

=35)

that is

Sham group

Sham+mdivi-1 group

ischemia group

and mdivi-1 group. Mouse model of acute myocardial ischemia was established by ligating left anterior descending branch in mice. SOD

MDA

ATP

ROS and markers of myocardial injury were measured

and myocardial and mitochorial morphology was observed to study the protective effect of mdivi-1 on the he

art of myocardial ischemia mice.

Results

The mice in the ischemia group showed damaged myocardial structure

more mitochondrial fragmentation

disordered arrangement

and obviously impaired mitochondrial function. While the treatment of mdivi-1 significantly reduced above damaged mitochondrial structure and function in myocardial cells

restored myocardial ATP (1.587±0.227 μmol/mg) and SOD (0.401±0.138 U/mg) contents (

0.05)

and decreased the production of ROS (4 276.0±687.5 fluorescent intensity/mg) and content of MDA (3.538±1.110 μmol/mg) (

0.05)

and thus alleviated the oxidative damages in the myocardium

reduced the levels of blood markers of myocardial injury

protected myocardial function

and finally significantly prolonged the survival time and improved the survival rate of myocardial ischemia mice.

Conclusion

Mitochondrial fission inhibitor mdivi-1 has a protective effect on myocardial ischemia mice.

关键词

Keywords

references

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