Applications of N6-(2-hydroxyethyl)adenosine in preparation of drugs for prevention or treatment of myocardial ischemic reperfusion injury

A technology for reperfusion injury and myocardial ischemia, applied in the field of biomedicine, can solve problems such as poor effect and damage to myocardial tissue, and achieve the effects of small side effects, myocardial protection, and anti-myocardial infarction damage

Pending Publication Date: 2018-07-27
ZHEJIANG SUB TROPICS CROP INST
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

[0005] The production and secretion of inflammatory factors and cell apoptosis also play an important role in myocardial reperfusion injury. These inflammatory reactions not only directly damage myocardial tissue, but also cause immune vascular damage, but by removing free oxygen (superoxide dismutation enzymes, reduced glutathione, etc.), improving the metabolism of ischemic tissue (such as Huxintong, Wanshuangli and other drugs), adding immunosuppressants, etc. to prevent and treat myocardial reperfusion injury are not effective in clinical application

Method used

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  • Applications of N6-(2-hydroxyethyl)adenosine in preparation of drugs for prevention or treatment of myocardial ischemic reperfusion injury
  • Applications of N6-(2-hydroxyethyl)adenosine in preparation of drugs for prevention or treatment of myocardial ischemic reperfusion injury
  • Applications of N6-(2-hydroxyethyl)adenosine in preparation of drugs for prevention or treatment of myocardial ischemic reperfusion injury

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Experimental program
Comparison scheme
Effect test

Embodiment 1H

[0038] The influence of embodiment 1HEA on cardiomyocyte viability

[0039] Experimental method: An in vitro cardiomyocyte sI / R model was constructed to confirm the effect of HEA on cardiomyocyte cell viability and autophagic flow.

[0040] This is done with the following steps:

[0041] 1) Spread cardiomyocytes H9c2 on a 96-well plate, and group as follows when the cell density reaches 80%: add 30ul / mL DMSO to the control group (because HEA needs DMSO to dissolve, so the control group adds DMSO equal to the dissolved HEA); the HEA group adds HEA (concentrations were 1ug / mL, 2.5ug / mL, 5ug / mL, 10ug / mL, 20ug / mL, 40ug / mL, 80ug / mL); treatment for 2h.

[0042] 2) After adopting the method established in (1), CCK-8 is used to detect the cell viability. The result is as figure 1 As shown, HEA less than 80ug / mL has no significant drug toxicity to the cells.

[0043] 3) Cardiomyocytes H9c2 were spread in 96-well plates, and when the cell density reached 80%, set a. Control group (...

Embodiment 2

[0047] Embodiment 2HEA is on the influence of physical and mental function

[0048] Experimental method: construct an in vivo myocardial cell ischemia / reperfusion model, and confirm the effect of HEA on cardiac function, myocardial infarction size, myocardial tissue lesion, myocardial cell apoptosis, myocardial autophagy level and inflammatory factors in blood

[0049] This is done with the following steps:

[0050] 1) The experimental S-D rats were grouped as follows:

[0051] a. Control group, treated with sham operation, only thoracotomy, threaded but not ligated in the left anterior descending branch

[0052] b.I / R group: ischemia-reperfusion group, ischemia 30min, reperfusion 120min

[0053] c. Ischemia-reperfusion + HEA intervention group (2.5mg / kg), intraperitoneal injection of HEA 15 minutes before ischemia, then ligation of the left anterior descending artery, myocardial ischemia for 30 minutes, and reperfusion for 120 minutes

[0054] d. Ischemia-reperfusion+HEA i...

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Abstract

The invention discloses applications of an active substance N6-(2-hydroxyethyl)adenosine (HEA) in Isaria cicadae Miquel, Cordyceps militaris, Cordyceps pruinosa and other Cordyceps in preparation of drugs for prevention or treatment of myocardial ischemic reperfusion injury. According to the present invention, the protection effect on myocardial ischemic reperfusion injury by HEA is developed through the cell model and the animal model; HEA can effectively improve the viability of cardiomyocytes after the hypoxia-reoxygenation treatment, and can induce the autophagy of cardiomyocytes and repair the autophagy flux; HEA can active the A1 receptor so as to effectively improve the cardiac function level of the rats after myocardial ischemic reperfusion, reduce the myocardial infarct size, reduce the apoptosis, improve the myocardial tissue morphology, repair the myocardial autophagy flux, and reduce the inflammatory reaction caused by myocardial ischemic reperfusion; and the multiple experiment results prove that HEA has anti-myocardial-ischemic-reperfusion-injury effect, such that HEA can be used for preventing and treating myocardial ischemic reperfusion injury and can provide important significance in the prevention of myocardial ischemia.

Description

technical field [0001] The invention belongs to the technical field of biomedicine, and specifically relates to the application of HEA in the preparation of drugs for preventing or treating myocardial ischemia-reperfusion injury. Background technique [0002] N6-(2-hydroxyethyl)adenosine [N(6)-(2-hydroxyethyl)-adenosine, HEA] is reported to exist in many kinds of Cordyceps cicadae and Cordyceps militaris, and is the first biological source It is a calcium ion antagonist with strong anti-ultraviolet radiation, anti-platelet aggregation and analgesic and anti-inflammatory effects. It has been proved by Chai Yiqiu that HEA has anti-convulsant, kidney-protecting and analgesic effects. However, there is no report on the effect of HEA on myocardial ischemia-reperfusion. It is expected to provide an effective, safe and multifunctional new drug for the prevention and treatment of ischemia-reperfusion injury if the relevant pharmacological effects and its mechanism of action are stu...

Claims

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Application Information

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IPC IPC(8): A61K31/7076A61P9/10A61P9/00
CPCA61K31/7076
Inventor 柴一秋章思思
Owner ZHEJIANG SUB TROPICS CROP INST
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