Abstract

Objective To explore the protective effects and mechanism of mild hypothermia treatment in the treatment of myocardial ischemia-reperfusion injury. Material and Methods. A total of 20 Sprague-Dawley (SD) rats were assigned to 4 groups: the blank control group, sham operation group, ischemia reperfusion group, and mild hypothermia therapy group (each n = 5). Some indexes were detected. In addition, myocardial cell models of oxygen-glucose deprivation/reoxygenation injury (OGD) were established. The expression of mRNA IL-6 and TNF-α and the key enzyme levels of apoptosis (cleaved-Caspase-3) and the NLRP3 inflammasome/p53 signaling pathway in the models were determined. Results The expression of serum IL-6 and TNF-α in the mild hypothermia therapy group was significantly lower than that in the ischemia reperfusion group. The mild hypothermia therapy group also showed a significantly lower TUNEL cell count and NLRP3 and p53 phosphorylation levels than the ischemia reperfusion group (all p < 0.05). The in vitro mild hypothermia + OGD group also showed significantly lower mRNA expression of IL-6 and TNF-α and levels of cleaved Caspase-3, NLRP3, and phosphorylated p53 protein than the OGD group (all p < 0.05). Conclusion In conclusion, mild hypothermia therapy can inhibit the apoptosis and myocardial inflammation of cells induced by MI/R injury in rats and inhibiting the activity of the NLRP3 inflammasome pathway and p53 signaling pathway may be the mechanism.

Highlights

  • Cardiovascular diseases are the leading cause of death in the world, which accounts for 25% of all causes of death worldwide in 2010 and 31% of all causes of death worldwide in 2016, and 85% cardiovascular disease-related deaths are caused by heart attack and stroke [1]

  • Acute myocardial infarction (AMI) is a myocardial necrosis event caused by unstable myocardial blood supply and is a primary cause of heart attack and stroke [3]

  • The pathophysiological mechanism of AMI is as follows: chronic atherosclerosis gives rise to coronary stenosis and atherosclerotic plaque disruption and causes plaques out from platelets that participate in blood circulation, resulting in the hypercoagulable state of blood vessels and rupture of other unstable plaques through feedback triggering, which eventually leads to irreversible necrosis of myocardial cells

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Summary

Introduction

Cardiovascular diseases are the leading cause of death in the world, which accounts for 25% of all causes of death worldwide in 2010 and 31% of all causes of death worldwide in 2016, and 85% cardiovascular disease-related deaths are caused by heart attack and stroke [1]. In China, cardiovascular diseases occupy the first place in the cause of death, accounting for about 40% of all causes of death. As a country with a large population, China is one of the countries with the heaviest medical burden for cardiovascular diseases in the world [2]. Acute myocardial infarction (AMI) is a myocardial necrosis event caused by unstable myocardial blood supply and is a primary cause of heart attack and stroke [3]. AMI is treated mainly by restoring the blood flow

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