| Object:To investigating the effection of intermittent aerobic exercise on CTRP3 gene and protein expression characteristic in rat tissues with or without myocardial infarction (MI); To further explore the possibility mechanism of intermittent aerobic exercise promote cardiac angiogenesis by affecting the expressions of CTRP3 in rats with myocardial infarction; Providing experimental evidence for the prevention and treatment of human heart disease.Materials and Methods:40 male 3-month-old SD rats were fed with the national standard rodent dry feed in a week. The rats were randomly divided into 5 groups(n=8, per group):control group(C), control+intermittent aerobic exercise group(CE), myocardial infarction group(MI), MI+intermittent aerobic exercise group (ME), sham group(S). MI and ME group was induced by ligation of the left anterior descending (LAD) coronary artery. S group do not ligation the LAD coronary artery. ME group rats started exercising at 1 week post-MI using a motorized rodent treadmill. Exercise in ME group was initiated at 10 m/min, for 10 min. Exercise intervals alternated between 7 min at 26 m/min of speed and 3 min at 15 m/min of speed, total time was 60 min. The exercise was performed 5 days per week for 8 weeks.After training, the following hemodynamic parameters were measured to detect cardiac function:LVSP, LVEDP, ądp/dtmax. The body weight, visceral white adipose tissue weight and heart coefficient was been measured. Then the heart was taken for histologic section and Masson dyeing. CTRP3mRNA and protein expression in the left ventricle was examined by RT-PCR and Western blot. Akt/pAkt and VEGF were examined by Western blot. Using immunofluoresence staining to measure angiogenesis.Results:(1) The epididymis and visceral white adipose tissue was the primary tissue of CTRP3 mRNA expression; The level of CTRP3 mRNA expression was significantly increased in myocardium, epididymis and visceral white adipose tissue with intermittent exercise intervention.(2) The myocardium, epididymis and visceral white adipose tissue was the primary tissue of CTRP3 protein expression; The level of CTRP3 protein expression was significantly increased in myocardium, epididymis and visceral white adipose tissue with intermittent exercise intervention.(3) The level of CTRP3 protein expression was significantly increased in rat serum after intermittent exercise.(4) pathological cardiac hypertrophy and the content of visceral fat was significantly improved in myocardial infarction rats after intermittent exercise. Varying degrees of cardiac hypertrophy in heart with myocardial infarction or intermittent exercise, intermittent exercise could reduce the degree of cardiac hypertrophy; Visceral fat accumulation in myocardial infarction rats, intermittent exercise could improve the visceral fat content in rats with myocardial infarction.(5) Expression level of CTRP3 mRNA in heart, aorta, epididymis, visceral adipose tissue, and brown adipose tissue was significantly increased in myocardial infarction rats. Expression level of CTRP3 mRNA in adipose tissue of myocardium, epididymis and viscera was significantly increased in myocardial infarction rats after intermittent exercise.(6) The level of CTRP3 protein expression was significantly improved in myocardial infarction rats after intermittent exercise. The level of CTRP3 protein expression was significantly decreased in myocardial infarction rats serum, the level of CTRP3 protein expression was significantly increased in myocardial infarction rats serum after intermittent exercise.(7) The level of CTRP3, pAkt and VEGF protein expression in heart was significantly improved with myocardial infarction rats after intermittent exercise. The level of CTRP3 protein expression was significantly decreased in myocardium with myocardial infarction rats, irritability activate Akt-VEGF signal, meanwhile myocardial ischemia and hypoxia stimulate HIF1-alpha expression.(8) Intermittent exercise promotes myocardial angiogenesis in myocardial infarction rats. Myocardial ischemia and hypoxia stimulate compensatory angiogenesis in the heart, intermittent exercise could significantly promote angiogenesis in ischemic myocardium, significantly increased the number of small arteries in the marginal zone of myocardial infarction in myocardial infarction rats, improvement of microcirculation in infarct area.(9) Intermittent exercise significantly reduced the level of myocardial apoptosis in myocardial infarction rats. The expression of Bax was significantly increased, the expression of Bcl-2 was significantly decreased, and the ratio of Bcl-2 to Bax was significantly increased; Intermittent exercise can significantly reduce the myocardial Bax expression, significantly increase the Bcl-2 expression, significantly reduce the ratio of Bcl-2 to Bax. Show that myocardial apoptosis was significantly increased after myocardial ischemia, intermittent exercise could significantly reduce the level of apoptosis of myocardial cells after myocardial infarction.(10) Intermittent exercise significantly reduced myocardial fibrosis and reduce the infarction area. MASSON staining showed that uneven distribution of myocardial cells in the marginal zone and non infarct zone of myocardial infarction, excessive proliferation of collagen fibers, myocardial collagen volume fraction CVF was significantly increased and alternative fibrosis; Intermittent exercise can significantly reduce myocardial fibrosis in rats with myocardial infarction, myocardial collagen volume fraction CVF was significantly decreased and reduce the infarction area.(11) Intermittent exercise significantly improves cardiac function in myocardial infarction. LVEDP significantly increased, LVSP and ądp/dt max significantly decreased after myocardial infarction; Intermittent exercise can significantly reduce the level of LVEDP and LVSP and ądp/dt max significantly increased. Shows that myocardial infarction seriously damages the heart function, intermittent exercise can significantly improve left ventricular systolic/diastolic function in rats with myocardial infarction.(12) Exercise improves cardiac function in myocardial infarction and exercise increased CTRP3 levels were positively correlated. Correlation analysis results shows that, the level of CTRP3 protein in visceral adipose tissue, serum and myocardium in rats and heart function were positively correlated.Indicate that the level of CTRP3 protein in the body is closely related to the cardiac function after myocardial infarction, suggest that adipose tissue secretion of CTRP3 to exert the protective effect of the heart by circulation.Conclusion:1.Intermittent exercise can significantly reduce pathological cardiac hypertrophy and visceral fat content in myocardial infarction rats, significantly increased myocardial, epididymis and visceral adipose tissue CTRP3 mRNA and protein expression and serum CTRP3 protein expression, upregulation of circulating CTRP 3 protein level.2.Intermittent exercise to further activate the pAkt-VEGF signal of myocardial infarction, improve myocardial ischemia and hypoxia, reduce the expression of HIF1-alpha; promote angiogenesis in ischemic myocardium, increase the number of small arteries in the marginal zone of myocardial infarction, and improve the microcirculation of the infarct area.3.Intermittent exercise can significantly reduce myocardial fibrosis in rats with myocardial infarction, myocardial collagen volume fraction CVF significantly reduced, and the infarct size; reduce the level of apoptosis of myocardial cells after myocardial infarction, and to improve the left ventricular systolic/diastolic function in rats with myocardial infarction.4.The level of CTRP3 protein in visceral adipose tissue, serum and myocardium of rats was positively correlated with cardiac function, and intermittent exercise was positively correlated with the CTRP3 level of myocardial infarction. Suggests that adipose tissue is secreted by CTRP3, which may exert a protective effect on the myocardium by circulation. |
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