Abstract
Objective To investigate the role of leptin in regulating cell inflammation and protecting myocardium after myocardial ischemia-reperfusion injury in rats through signaling pathway at tissue and molecular protein levels. Methods Healthy female SD rats were randomly divided into 4 groups, which were sham, I/R group, leptin low-dose intervention group, and high-dose intervention group (40 μg/kg and 80 μg/kg, respectively). Cardiac hemodynamics, myocardial enzymology, inflammatory indices, and pathological changes were observed. Western blot was used to observe the expression of PI3K, AKT, and NFκB protein by leptin. Results Leptin can improve the hemodynamics of cardiac ischemia-reperfusion rats, improve the expression of myocardial enzymology, reduce the release of cardiac and serum inflammatory factors, increased PI3k, AKT, and NFκB expression, and reduce the occurrence of inflammation from the perspective of gross pathology, thus protecting the body. Conclusion Leptin pretreatment can reduce MIRI injury, and the protective mechanism may be that leptin upregulates PI3K-AKT-NFκB expression in myocardial tissue to reduce inflammation and promote repair of I/R injury.
Highlights
Over the past 40 years, the global death rate from coronary heart disease has decreased; about a third or more of deaths from coronary heart disease occur in people over 35 [2]
The significance of this study is to further explore the regulatory and protective effects of leptin on Myocardial ischemic reperfusion injury (MIRI) in rats through inflammatory signaling pathways at tissue molecular level and protein pathway
After 30 min of ischemia-reperfusion, the hemodynamic indexes of isolated heart in I/R group were significantly changed compared with the blank group, in which the maximum rate of increase of left ventricular pressure (+dp/dt max) and the maximum rate of decrease of left ventricular pressure (-dp/ dt max) were significantly decreased (p < 0:05)
Summary
To investigate the role of leptin in regulating cell inflammation and protecting myocardium after myocardial ischemiareperfusion injury in rats through signaling pathway at tissue and molecular protein levels. Myocardial enzymology, inflammatory indices, and pathological changes were observed. Western blot was used to observe the expression of PI3K, AKT, and NFκB protein by leptin. Leptin can improve the hemodynamics of cardiac ischemia-reperfusion rats, improve the expression of myocardial enzymology, reduce the release of cardiac and serum inflammatory factors, increased PI3k, AKT, and NFκB expression, and reduce the occurrence of inflammation from the perspective of gross pathology, protecting the body. Leptin pretreatment can reduce MIRI injury, and the protective mechanism may be that leptin upregulates PI3KAKT-NFκB expression in myocardial tissue to reduce inflammation and promote repair of I/R injury
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