Cardioprotective effects mitochondrial ATP-sensitive potassium channel in exercise conditioning

Peng, Feng-Lin; Guo, Yuanyuan; Mo, W.-B.; Xu, Simao; Hui-fang, Liao

doi:10.4238/2014.september.12.17

Cited by 5 publications

(2 citation statements)

References 16 publications

(18 reference statements)

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“…Cardiac function depends on the ventricular systolic and diastolic functions [ 19 ]. Recent studies have demonstrated that myocardial I/R injury may induce the changes of cardiac hemodynamic parameters and then affect cardiac function [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

Penehyclidine Hydrochloride Preconditioning Provides Cardioprotection in a Rat Model of Myocardial Ischemia/Reperfusion Injury

Lin

et al. 2015

PLoS ONE

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To investigate the impacts and related mechanisms of penehyclidine hydrochloride (PHC) on ischemia/reperfusion (I/R)-induced myocardial injury. A rat model of myocardial I/R injury was established by the ligation of left anterior descending coronary artery for 30 min followed by 3 h perfusion. Before I/R, the rats were pretreated with or without PHC. Cardiac function was measured by echocardiography. The activities/levels of myocardial enzymes, oxidants and antioxidant enzymes were detected. Evans blue/TTC double staining was performed to assess infarct size. Cardiomyocyte apoptosis was evaluated by TUNEL assay. The release of inflammatory cytokines and inflammatory mediators was detected by ELISA. Western blot was performed to analyze the expression of COX-2, IκB, p-IκB and NF-κB. Meanwhile, the rats were given a single injection of H-PHC before I/R. The effects of PHC on myocardial infarct and cardiac function were investigated after 7 days post-reperfusion. We found that PHC remarkably improved cardiac function, alleviated myocardial injury by decreasing myocardial enzyme levels and attenuated oxidative stress in a dose-dependent manner. Additionally, PHC preconditioning significantly reduced infarct size and the apoptotic rate of cardiomyocytes. Administration of PHC significantly decreased serum TNF-α, IL-1β, IL-6 and PGE2 levels and myocardium COX-2 level. Meanwhile, the expression levels of p-IκB and NF-κB were downregulated, while IκB expression was upregulated. H-PHC also exerted long-term cardioprotection in a rat model of I/R injury by decreasing infarct size and improving cardiac function. These results suggest that PHC can efficiently protect the rats against I/R-induced myocardial injury.

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Section: Discussionmentioning

confidence: 99%

Penehyclidine Hydrochloride Preconditioning Provides Cardioprotection in a Rat Model of Myocardial Ischemia/Reperfusion Injury

Lin

et al. 2015

PLoS ONE

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“…Mitochondrial-derived ROS are prominent early drivers of ischemia-reperfusion injury and have been considered the consequence of the interaction of dysfunctional respiratory chain with O 2 during reperfusion (37). Previous studies have revealed that exercise preconditioning improved myocardial tolerance to ischemia by activating mitochondrial ATP-sensitive K + channels (38,39). Moreover, the protective effects of exercise training on cardiovascular systems are associated with up-regulating the expression of antioxidant enzymes and stress-related proteins (40,41).…”

Section: Discussionmentioning

confidence: 99%

Exercise Training Improves Mitochondrial Bioenergetics of Natural Killer Cells

Lin

Hsu

et al. 2021

Medicine &Amp; Science in Sports &Amp; Exercise

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IntroductionMitochondrial bioenergetics is critical for immune function in natural killer (NK) cell. Physical exercise modulates NK cell functionality, depending on the intensity and type of exercise. This study elucidates how interval and continuous exercise regimens affect the phenotypes and mitochondrial bioenergetics of NK cells.MethodsSixty healthy sedentary males were randomly assigned to engage in either high-intensity interval training (HIIT, 3-min intervals at 80% and 40% maximal O2, n = 20; age, 22.2 yr; body mass index [BMI], 24.3 kg·m−2) or moderate-intensity continuous training (MICT, sustained 60% maximal O2, n = 20; age, 22.3 yr; BMI, 23.3 kg·m−2) for 30 min·d−1, 5 d·wk−1 for 6 wk or were assigned to a control group that did not receive exercise intervention (n = 20; age, 22.6 yr; BMI, 24.0 kg·m−2). Natural killer cell phenotypes, granule proteins, and mitochondrial oxidative stress/oxidative phosphorylation after graded exercise test (GXT) were measured before and after the various interventions.ResultsBefore the intervention, the GXT increased the mobilization of CD57+NK cells into the blood and elevated mitochondrial matrix oxidant burden (MOB) in NK cells, Following the 6 wk of interventions, both HIIT and MICT (i) diminished mobilization of CD57+NK cells into the blood and depressed mitochondrial MOB level in NK cells immediately after GXT, (ii) increased mitochondrial membrane potential and cellular perforin and granzyme B levels in NK cells, and (iii) enhanced the maximal and reserve O2 consumption rates and heightened bioenergetic health index in NK cells. In addition, HIIT increased maximal work rate than those of MICT.ConclusionsEither HIIT or MICT increases the expressions of cytotoxic granule proteins and depresses mitochondrial MOB elevated by GXT, along with improving mitochondrial bioenergetic functionality in NK cells. Moreover, HIIT is superior to MICT in improving aerobic capacity.

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Cardiac Ischemia/Reperfusion Injury: The Beneficial Effects of Exercise

Borges

Verdoorn

2017

Advances in Experimental Medicine and Biology

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Cardiac ischemia reperfusion injury (IRI) occurs when the myocardium is revascularized after an episode of limited or absent blood supply. Many changes, including free radical production, calcium overload, protease activation, altered membrane lipids and leukocyte activation, contribute to IRI-induced myocardium damage. Aerobic exercise is the only countermeasure against IRI that can be sustained on a regular basis in clinical practice. Interestingly, both short-term (3-5 days) and long-term (several weeks) exercise increase myocardial tolerance, reduce infarct size area and arrhythmias induced by IRI. Exercise protects the heart against IRI in a biphasic manner. The early phase of cardioprotection occurs between 30 min and 3 h following an acute exercise bout, whilst the late phase is achieved within 24 h after the exercise bout and persists for several days. As for the exercise intensity, although controversial data exists, it is feasible that the amount of cardioprotection is proportional to exercise intensity and only achieved above a critical threshold. It is known that aerobic exercise produces a cardioprotective phenotype, however the mechanisms responsible for this phenomenon remain unclear. Apparently, aerobic exercise-induced preconditioning is dependent on several factors that work together to protect the heart. Altered nitric oxide (NO) signaling, increased levels of heat shock proteins (HSPs), enhanced function of ATP-sensitive potassium channels, increased activation of opioids system, and enhanced antioxidant capacity may contribute to exercise-induced cardioprotection. Much has been discovered from animal models involving exercise-induced cardioprotection against cardiac IRI, however translating these findings to clinical practice still represents the major challenge in this field.

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Cardioprotective effects mitochondrial ATP-sensitive potassium channel in exercise conditioning

Cited by 5 publications

References 16 publications

Penehyclidine Hydrochloride Preconditioning Provides Cardioprotection in a Rat Model of Myocardial Ischemia/Reperfusion Injury

Penehyclidine Hydrochloride Preconditioning Provides Cardioprotection in a Rat Model of Myocardial Ischemia/Reperfusion Injury

Exercise Training Improves Mitochondrial Bioenergetics of Natural Killer Cells

Cardiac Ischemia/Reperfusion Injury: The Beneficial Effects of Exercise

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