Electroacupuncture At PC6 Modulates Inflammation In Myocardial Infarcted Rats

Objective:Myocardial infarction(MI)is a significant public health issue and a major cause of global mortality and morbidity.Survivors of MI are at an increased risk of dying from heart failure.The risk of heart failure and poor prognosis for MI patients are largely related to the extent of myocardial injury and infarct size.A major factor that increases infarct size and impairs the repair process of the post-infarcted heart is inflammation.In MI,inflammation is characterized as excessive,widespread,and prolonged.It is also associated with increased levels of oxidative stress and neurohormonal activities,which further aggravate myocardial injury.In recent research,there has been a growing interest in targeting macrophage polarization to modulate inflammation.Attenuating inflammation and promoting the polarization of anti-inflammatory M2 macrophages have been suggested as a potential therapeutic strategy for improving myocardial repair and clinical outcomes of MI patients.In previous stu.dies,electroacupuncture(EA)has been shown to moderate inflammation and exert beneficial effects in various heart-related conditions,but its mechanism of action and immune-modulating effects on MI are still unclear.Therefore,the present study aimed to investigate whether EA is effective in mitigating myocardial injury and inflammatory reaction as well as oxidative stress and neurohormonal activities in MI.establishedMethods:MI model was in Sprague-Dawley rats by surgical occlusion of the left anterior descending(LAD)coronary artery.The infarcted rats were randomly divided into either no intervention group(MI,n=10)or electroacupuncture group(MI+EA,n=10).Sham operated rats served as the control group(SO,n=10).EA was performed at bilateral PC6(neiguan)for 20 minutes.Four hours later,serum and myocardial tissue samples were collected and evaluated to determine the extent of myocardial injury,inflammation,oxidative stress,and neurohormonal activities.Results:EA intervention was effective in attenuating myocardial injury compared to the non-treated infarcted group,as assessed by decreased levels of myocardial enzymes.EA reduced the release of pro-inflammatory cytokines,TNF-a,IL-1?,and IL-6,and suppressed the activation of NF-KB and CaMK?.It also promoted the polarization of macrophages towards the anti-inflammatory M2 subtype and reduced the expression of the pro-inflammatory M1 subtype in the border zone.Outcome measures for oxidative stress and hyperactivity of the sympathetic nervous system and renin-angiotensin system were also modulated by the EA intervention.Discussion:Excessive inflammation in MI has been found to exacerbate myocardial injury and infarct size,thereby worsening the clinical outcomes of MI patients.The present study demonstrates that EA can effectively modulate inflammation by suppressing both NF-KB and pro-inflammatory cytokines.The study findings also provided new insight about the ability of EA to regulate macrophage polarization in MI.The beneficial effects of EA for MI are further corroborated by improvements in oxidative stress and neurohormonal activities.