https://doi.org/10.4081/jsas.2011.567

BRAIN DAMAGE AND OXIDATIVE STRESS IN THE PERINATAL PERIOD: MELATONIN AS A NEUROPROTECTIVE NEW DRUG

Vol. 3 No. 1 (2011)
Submitted: 20 August 2012
Accepted: 20 August 2012
Published: 20 August 2012
oxidative stress, hypoxia-ischemia, animal model, melatonin
Abstract Views: 838
PDF: 1013
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Authors

S. Perrone
Department of Pediatrics, Obstetrics and Reproductive Medicine, University of Siena, Italy.
S. Bertrando
Department of Pediatrics, Obstetrics and Reproductive Medicine, University of Siena, Italy.
S. Cornacchione
Department of Pediatrics, Obstetrics and Reproductive Medicine, University of Siena, Italy.
S. Negro
Department of Pediatrics, Obstetrics and Reproductive Medicine, University of Siena, Italy.
M.L. Tataranno
Department of Pediatrics, Obstetrics and Reproductive Medicine, University of Siena, Italy.
M. Tei
Department of Pediatrics, Obstetrics and Reproductive Medicine, University of Siena, Italy.
G. Stazzoni
Department of Pediatrics, Obstetrics and Reproductive Medicine, University of Siena, Italy.
G. Buonocore
buonocore@unisi.it
Department of Pediatrics, Obstetrics and Reproductive Medicine, University of Siena, Italy.
Prenatal factors represent the main determinants of hypoxicischemic encephalopathy (HIE) rather than intra- or post-partum conditions in perinatal period. Oxidative stress (OS) plays a key role in perinatal brain damage. The development of therapeutic strategies to improve the outcomes of babies with HIE is still mandatory. Aim: to evaluate the effectiveness of melatonin as a neuroprotective drug. To investigate the influence of Melatonin on the OS biomarkers production in an animal model of cerebral hypoxia-ischemia. Methods: 30 rat pups were subjected to ligation of the right common carotid artery and exposed for 2.5 hours at an hypoxic condition. A group of 15 rats was administered melatonin at a dose of 15 mg/kg 5 minutes after the procedure (Mel GROUP). At the same time 15 rats received placebo (HI GROUP). A group of 5 healthy rats was used as sham operated (S GROUP). Isoprostanes (IsoPs), neuroprostanes (NPs) and neurofurans (NFs), all markers of OS were measured at 1, 24 and 48 h from ischemic injury in homogenized cerebral cortex of the two sides, right (hypoxia and ischemia) and left (hypoxia). Results: In the HI group were observed: a significant increase of IsoPs on the left side of cortex after 1 h from HI injury (p<0.001); a significant increase of NPs on both sides after 24 h (p<0.05) and a significant increase of NFs on the left (p<0.05) after 24 h. After 48 h in the Mel group was observed a significant increase of IsoPs on the left (p<0.05) and of NPs on both sides of cerebral cortex (p<0.05). Conclusions: Melatonin reduces OS biomarkers in cerebral cortex of HI rats after 24 h from its administration. The drug is no longer effective after 48 h. These results lay the groundwork for future clinical studies in infants.

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How to Cite

Perrone, S., Bertrando, S., Cornacchione, S., Negro, S., Tataranno, M., Tei, M., Stazzoni, G., & Buonocore, G. (2012). BRAIN DAMAGE AND OXIDATIVE STRESS IN THE PERINATAL PERIOD: MELATONIN AS A NEUROPROTECTIVE NEW DRUG. Journal of the Siena Academy of Sciences, 3(1), 34–37. https://doi.org/10.4081/jsas.2011.567

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