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Netrin-1 plays a role in the effect of 10 weeks moderate exercise on myocardial fibrosis in rats
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Abstract
This study aimed to determine the effect of Netrin-1 and its receptor on acute myocardial infarction in rats after aerobic exercise.METHODS:Twenty-four rats were randomly divided into three groups: the sham group (n = 8); acute myocardial infarction model group (AMI)(n = 8); and aerobic exercise treatment after acute myocardial infarction group(ET) (n = 8). After 10 weeks, the levels of netrin-1, tumor necrosis factor alpha α(TNF-α), and interleukin 6(IL-6) in the serum were measured. The expression of matrix metalloproteinases 2 and 9(MMP2,9), and their inhibitor, tissue inhibitor of metalloproteinases 2(TIMP2), myocardial netrin-1, Deleted in colorectal cancer(DCC) receptor were evaluated. Histopathological were evaluated. The collagen volume fraction of myocardial tissues was also calculated.RESULTS:Compared to the sham group, the AMI group and ET groups showed increased levels of serum TNF-α, IL-6 and significantly reduced levels of netrin-1. Levels of TNF-α and IL-6 were significantly reduced in the ET group compared to the AMI group, whereas the level of netrin-1 was increased. The expression of myocardial MMP2,9 was significantly increased in the AMI group compared to the sham group, whereas that of myocardial netrin-1, inhibitor of TIMP2 and DCC receptor, was significantly reduced. Compared to AMI group, the ET group showed reduced expression of myocardial MMP2,9 proteins, whereas expression of myocardial netrin-1, inhibitor of TIMP2 and DCC receptor, was significantly increased. The collagen volume fraction of myocardial tissues was significantly increased in the AMI group and ET group compared to the sham group, with the greater increase being noted in the AMI group.CONCLUSIONS: Aerobic exercise could increase levels of serum netrin-1 myocardial netrin-1, and DCC receptor and reduced expression of myocardial MMP2,9 proteins, to improve the degree of fibrosis following myocardial infarction in rats.
Title: Netrin-1 plays a role in the effect of 10 weeks moderate exercise on myocardial fibrosis in rats
Description:
Abstract
This study aimed to determine the effect of Netrin-1 and its receptor on acute myocardial infarction in rats after aerobic exercise.
METHODS:Twenty-four rats were randomly divided into three groups: the sham group (n = 8); acute myocardial infarction model group (AMI)(n = 8); and aerobic exercise treatment after acute myocardial infarction group(ET) (n = 8).
After 10 weeks, the levels of netrin-1, tumor necrosis factor alpha α(TNF-α), and interleukin 6(IL-6) in the serum were measured.
The expression of matrix metalloproteinases 2 and 9(MMP2,9), and their inhibitor, tissue inhibitor of metalloproteinases 2(TIMP2), myocardial netrin-1, Deleted in colorectal cancer(DCC) receptor were evaluated.
Histopathological were evaluated.
The collagen volume fraction of myocardial tissues was also calculated.
RESULTS:Compared to the sham group, the AMI group and ET groups showed increased levels of serum TNF-α, IL-6 and significantly reduced levels of netrin-1.
Levels of TNF-α and IL-6 were significantly reduced in the ET group compared to the AMI group, whereas the level of netrin-1 was increased.
The expression of myocardial MMP2,9 was significantly increased in the AMI group compared to the sham group, whereas that of myocardial netrin-1, inhibitor of TIMP2 and DCC receptor, was significantly reduced.
Compared to AMI group, the ET group showed reduced expression of myocardial MMP2,9 proteins, whereas expression of myocardial netrin-1, inhibitor of TIMP2 and DCC receptor, was significantly increased.
The collagen volume fraction of myocardial tissues was significantly increased in the AMI group and ET group compared to the sham group, with the greater increase being noted in the AMI group.
CONCLUSIONS: Aerobic exercise could increase levels of serum netrin-1 myocardial netrin-1, and DCC receptor and reduced expression of myocardial MMP2,9 proteins, to improve the degree of fibrosis following myocardial infarction in rats.
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