Melatonin alleviates asphyxial cardiac arrest-induced cerebellar Purkinje cell death by attenuation of oxidative stress.
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
melatonin | increase | neuroprotective effects following ischemia/reperfusion-induced brain injury | animal models | - | appears to promote | #1 |
melatonin treatment | increase | survival rate | vehicle-treated asphyxial CA/CPR rats | ≥40% vs 10% | significantly improved | #2 |
melatonin treatment | decrease | neurological deficit | vehicle-treated asphyxial CA/CPR rats | - | significantly improved | #3 |
melatonin treatment | decrease | asphyxial CA/CPR-induced Purkinje cell death | vehicle-treated asphyxial CA/CPR rats | - | exhibited protective effect against | #4 |
melatonin | decrease | autophagy-like processes (Beclin-1, Atg7 and LC3) | - | - | remarkable attenuation of | #5 |
melatonin | decrease | superoxide anion radical (O | - | - | dramatic reduction in | #6 |
Although multiple reports using animal models have confirmed that melatonin appears to promote neuroprotective effects following ischemia/reperfusion-induced brain injury, the relationship between its protective effects and activation of autophagy in Purkinje cells following asphyxial cardiac arrest and cardiopulmonary resuscitation (CA/CPR) remains unclear. Rats used in this study were randomly assigned to 6 groups as follows; vehicle-treated sham operated group, vehicle-treated asphyxial CA/CPR operated group, melatonin-treated sham operated group, melatonin-treated asphyxial CA/CPR operated group, PDOT (a MT2 melatonin receptor antagonist) plus (+) melatonin-treated sham operated group and PDOT+melatonin-treated asphyxial CA/CPR operated group. Melatonin (20 mg/kg, i.p., 4 times before CA and 3 times after CA) treatment significantly improved survival rate and neurological deficit compared with the vehicle-treated asphyxial CA/CPR rats (survival rates ≥40% vs 10%), showing that melatonin treatment exhibited protective effect against asphyxial CA/CPR-induced Purkinje cell death. The protective effect of melatonin against CA/CPR-induced Purkinje cell death paralleled a remarkable attenuation of autophagy-like processes (Beclin-1, Atg7 and LC3), as well as a dramatic reduction in superoxide anion radical (O