Mechanism of melatonin through paraventricular nucleus against myocardial ischemia/reperfusion injury

  AIM  To explore the mechanism of peripheral injection of melatonin in regulating sympathetic activity through hypothalamic paraventricular nucleus (PVN) against myocardial I/R injury.

  METHODS  The myocardial I/R injury model of C57BL/6J MICE was established 24 hours after intraperitoneal injection of melatonin or sterile saline. T cardiac functions were measured by echocardiography and the infarct size was measured by Evans blue/TTC double staining after 24 hours of reperfusion. The levels of Il-10 and il-1β in paraventricular nucleus of hypothalamus were detected by immunofluorescence assay, the levels of NF-κb in paraventricular nucleus of hypothalamus and myocardial Tyrosine 3-monooxygenase were detected by Western blot and the level of (-)-noradrenaline in plasma was detected by ELISA.

  RESULTS  Peripheral administration of melatonin inhibited NF-ΚB level in PVN region, decreased IL-1 β level in PVN region, increased IL-10 level, decreased NE and TH activity, reduced infarct size （all P<0.01） and improved cardiac functions in C57BL/6J mice.

  CONCLUSION  Peripheral injection of melatonin can regulate the level of inflammatory cytokines in PVN, inhibit the activity of sympathetic nervous system and improve the cardiac function decline induced by myocardial I/R injury.