Objective
To investigate the influence of aerobic exercise on myocardial injury, NF-B expression, glucolipid metabolism and inflammatory factors in rats with Coronary Heart Disease (CHD) and explore the possible causative role.

Methods
۴۵ Sprague Dawley® rats were randomized into model, control and experimental groups. A high-fat diet was adopted for generating a rat CHD model, and the experimental group was given a 4-week aerobic exercise intervention. ECG was utilized to evaluate the cardiac function of the rats; HE staining to evaluate the damage of myocardial tissue; TUNEL staining to evaluate cardiomyocyte apoptosis level; ELISA to assay the contents of inflammatory factors and glucolipid metabolism in cardiomyocytes; qPCR to assay IB- and NF-B mRNA expression; Western-blot to assay the apoptosis-related proteins and NF-B signaling pathway-related proteins expressions in myocardial tissue.

Results
In contrast to the model group, aerobic exercise strongly improved the rat’s cardiac function and glucolipid metabolism (p < 0.01), enhanced IL-10 content, Bcl-2/Bax level as well as IB- protein and mRNA expression (p < 0.01), and reduced myocardial injury and cardiomyocyte apoptosis, the contents of IL-6, IL-1 and TNF-, Caspase 3 level, NF-B mRNA and protein expression and p-p38 and p-STAT3 expressions (p < 0.01).

Conclusion
Aerobic exercise can not only effectively reduce myocardial injury, the release of inflammatory factors and NF-B expression in CHD rats, but also improve cardiac function and glucolipid metabolism. Its mechanism is likely to be related to the inhibition of the NF-B signaling pathway.

Introduction

Coronary Heart Disease (CHD) refers to coronary artery lumen stenosis or even blockage caused by atherosclerosis, which causes myocardial ischemia, hypoxia and even necrosis, and is also known as ischemic heart disease. 1 , 2 Physiological, genetic and environmental factors that cause aberrant glucolipid metabolism and inflammatory response disorders are the dominating incentives that induce atherosclerosis and the primary pathophysiological basis of CHD. 3 , 4 With the improvement in living standards, the incidence of CHD is increasing year by year, posing a huge economic burden on families and countries. Reducing the mortality and extending the survival time of CHD patients is a major challenge that cardiovascular disease researchers and clinicians urgently need to solve.

Considerable evidence shows that vascular endothelial injury will raise the adhesion and permeability of vascular endothelium, and then multiple inflammatory factors will gather and produce an inflammatory fiber proliferation reaction, which eventually gives rise to atherosclerosis. 7 , 8 , 9 Nuclear Factor Kappa B (NF-B) takes part in not only the occurrence but also the development of inflammatory response. NF-B inhibitor protein IB- can accelerate the dissociation of NF-B. The dissociated NF-B can be rapidly transferred to the nucleus, modulating the transcription and translation processes of diverse inflammatory factors and adhesion factors, and is an important cytokine that modulates the activation and cascade amplification of inflammatory factors. 10 , 11 Schiffmann et al. 12 have demonstrated that CHD patients will have apparent glucolipid metabolism disorder. Over-nutrition and sedentary behaviors will strikingly accelerate the accumulation of fat and glucose in the body, which in turn will aggravate the vascular endothelial damage of patients. Substantial evidence indicates that aerobic exercise can efficaciously regulate glucolipid metabolism in the body, reduce the activity of lipoprotein lipase, lower blood lipid and blood sugar levels, and reduce body weight. 13 , 14 Ornish et al. 15 demonstrated that long-term aerobic exercise can apparently reduce blood lipid levels and reduce vascular endothelial damage in patients with cardiovascular disease. At present, there are few studies on the impact of aerobic exercise on myocardial damage, glucolipid metabolism, and inflammation in CHD. This investigation aimed to build a rat CHD model to study the influence of aerobic exercise on myocardial damage, NF-B expression, glucolipid metabolism and inflammatory responses in CHD rats, as well as to further explore its possible causative role.