Research method of MS-275 acting on acute myocardial ischemia reperfusion injury

A technology of acute myocardial ischemia and MS-275, which is applied in the medical field and can solve problems such as less research on molecular mechanisms

Pending Publication Date: 2020-08-25
THE SECOND XIANGYA HOSPITAL OF CENT SOUTH UNIV
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  • Claims
  • Application Information

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Problems solved by technology

However, the specific molecular mechanisms involve

Method used

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Embodiment

[0016] The research method of MS-275 acting on acute myocardial ischemia-reperfusion injury comprises the following steps:

[0017] Step 1: Establish a rat acute MI / RI model by ligation of the left anterior descending coronary artery in SD male rats: 72 SD male rats were randomly divided into 4 groups, 18 in each group: the first group was Sham operation group (Sham group), only threading without ligation; the second group is ischemia 30 minutes group (I 30min group); the third group is ischemia 30 minutes reperfusion 60 minutes group (I / R60min group); The group was ischemia for 30 minutes and reperfusion for 2 hours (I / R 120min group); after the experiment, the rats were executed, the heart was separated, and the tissue samples of the myocardial infarction area were taken, and the section was stained to observe the range of myocardial infarction and the cell tissue of the myocardial infarction area. Morphological changes, and histone acetylation level, HDAC1 and miR-210 expre...

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Abstract

The invention discloses a research method of MS-275 acting on acute myocardial ischemia reperfusion injury. The research method comprises the following steps: step I, performing ligation of an anterior descending branch of a left coronary artery of an SD male bandicoot to construct a bandicoot acute MI/RI model; step II, observing the action of the MS-275 in an MI/RI acute stage of the bandicoot;and step III, discussing a molecular mechanism of the MS-275 on bandicoot MI/RI protection action. According to the research, through constructing the bandicoot acute MI/RI model and combination within vivo and vitro experiments, the following research objectives are achieved: (1) observing the acetylation level of histone, and expression of HDAC1 and microRNA-210(miR-210) in cardiac muscle tissue of the bandicoot at the MI/RI acute stage; (2) confirming that the MS-275, a novel HDACI type selective depressant, has protection action on MI/RI of the bandicoot and influence on the acetylation level of the histone and expression of HDAC1 and miR-210 in tissue of a myocardial infarction region of the bandicoot subjected to myocardial ischemia reperfusion; and (3) disclosing a specific molecular mechanism that the MS-275 improves MI/RI of the bandicoot from the angle of miRNA epigenetic regulation, and providing an important theory and experiment basis for MI/RI treatment with HDACi.

Description

technical field [0001] The invention relates to the field of medical technology, in particular to a research method of MS-275 acting on acute myocardial ischemia-reperfusion injury. Background technique [0002] A large number of studies have shown that histone deacetylase, as an important regulator of epigenetic modification, is involved in the pathogenesis of myocardial ischemia / reperfusion injury. Histone deacetylase inhibitors can interfere with the function of HDACs, effectively reduce ischemia / reperfusion injury, and have broad therapeutic prospects in the field of myocardial protection. However, the specific molecular mechanisms involved in this protective effect are less studied. Contents of the invention [0003] In order to overcome the above problems, the present invention provides a research method for MS-275 acting on acute myocardial ischemia-reperfusion injury. [0004] The technical scheme adopted in the present invention is: [0005] The research method...

Claims

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Application Information

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IPC IPC(8): C12Q1/6883C12Q1/686G01N33/68A61K49/00
CPCC12Q1/6883C12Q1/686G01N33/68A61K49/0008C12Q2600/178G01N2800/2871C12Q2561/113
Inventor 郭斌李朵徐军美
Owner THE SECOND XIANGYA HOSPITAL OF CENT SOUTH UNIV
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