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Published on: April 16, 2018
Protective effects of melatonin on ischemia-reperfusion induced myocardial damage and hemodynamic recovery in rats
1Department of Obstetrics and Gynecology, the Second Affiliated Hospital of Soochow University, Suzhou, China. weipeizhucn@163.com.
Aim:
To investigate the mechanism of melatonin (MT) protection of adult rate myocardial ischemia-reperfusion injury and its influence on rat's hemodynamic recovery.
Materials And Methods:
48 rats were randomly divided into MT group (n=36) and the control group (n=12), MT group was divided into three sub-groups according to different dosages: Group I (n=12) was administered with 2.5 mg/kg MT; Group II (n=12) was administered with 5 mg/kg MT; Group III (n=12) was administered with 10 mg/kg MT. The electrocardiogram of four groups was observed with the left coronary artery blocked for 10min at first and then reperfused for 15min. Hemodynamic evolving was observed and changes in energy metabolism of rat myocardium were monitored. TUNEL and immunohistochemistry were applied to detect the cell apoptosis index, protein expression of Bcl-2 and Bax.
Results:
LVDP (left ventricular developed pressure) and ± dp/dt in MT group presented better recovery at various time points than the control group. Among them, Group III had the optimal recovery degree (p < 0.05). After MT administration, ATP content in myocardial cells in MT group was significantly higher than the control group. Compared with the control group, the concentration of mitochondrial MDA and Ca2+ in myocardial cells in MT group showed a downward trend. But its GSH concentration was significantly higher than the control group (p < 0.05). The improvement degree of ATP, MDA, GSH and Ca2+ concentration in Group II over-performed Group I (p < 0.05). MT-intervened myocardial apoptosis index (AI) and Bax positive expression index declined while Bcl-2 positive expression index increased (p < 0.01).
Conclusions:
MT effectively inhibited myocardial apoptosis during the myocardial ischemia-reperfusion of rats, protected the structural integrity of mitochondria in myocardial cells, promoted ATP synthesis, and avoided heart damage in many ways. This protection mechanism was related with anti-oxidative damage. Meanwhile, MT could promote the hemodynamic recovery after myocardial ischemia-reperfusion in rats.
Insights
Melatonin (MT) effectively protects against rat myocardial ischemia-reperfusion injury by reducing apoptosis and improving energy metabolism. This treatment promotes better hemodynamic recovery following heart damage.
Area of Science:
- Cardiovascular Research
- Cellular Biology
- Pharmacology
Background:
- Myocardial ischemia-reperfusion (I/R) injury is a significant clinical concern.
- Melatonin (MT) is a hormone with known antioxidant properties.
Purpose of the Study:
- To investigate the protective mechanisms of melatonin against myocardial I/R injury in rats.
- To assess melatonin's influence on hemodynamic recovery after I/R.
Main Methods:
- Adult rats underwent left coronary artery occlusion followed by reperfusion.
- Rats were treated with varying doses of melatonin (2.5, 5, or 10 mg/kg) or a control.
- Hemodynamic parameters, myocardial energy metabolism (ATP, MDA, GSH, Ca2+), and apoptosis (TUNEL, Bcl-2, Bax) were evaluated.
Main Results:
- Melatonin treatment significantly improved left ventricular developed pressure and ±dp/dt recovery compared to controls.
- Melatonin increased myocardial ATP and GSH levels while decreasing MDA and Ca2+ concentrations.
- Melatonin administration reduced myocardial apoptosis index and Bax expression, and increased Bcl-2 expression.
Conclusions:
- Melatonin effectively inhibits myocardial apoptosis and protects mitochondrial integrity during I/R injury.
- The protective effects are linked to anti-oxidative damage mechanisms.
- Melatonin promotes hemodynamic recovery post-myocardial I/R in rats.
