Abstract
Neonatal hypoxic-ischemic brain injury is a devastating disease with limited treatment options. Preventive treatment with resveratrol has indicated to be well tolerated and has lower toxicity in both experimental models and human patients. However, whether resveratrol administration post-hypoxic-ischemic protects against neonatal hypoxic-ischemic injury is not known. Here we reported that post-treatment with resveratrol significantly reduced brain damage at 7-day after the injury. We found that resveratrol reduced the expression levels of key inflammatory factors at the mRNA and protein levels, and at least partially via inhibiting microglia activation. Moreover, resveratrol exerted an anti-apoptotic effect, as assessed by TUNEL staining, and altered the expression of the apoptosis-related genes Bax, Bcl-2 and caspase3. Our data indicate that post-treatment with resveratrol protects against neonatal hypoxic-ischemic brain injury and suggest a promising therapeutic strategy to this disease.
Highlights
Neonatal encephalopathy due to perinatal hypoxiaischemia (HI) is a devastating disease that is a main cause of mortality in infants
We found that post-treatment with resveratrol has a neuroprotective effect on neonatal hypoxicischemic brain injury and that the effect is related to the inhibition of inflammation and apoptosis
We found that post-treatment with resveratrol significantly reduced brain damage, decreased the protein levels of key inflammatory factors, and altered the expression of the apoptosis-related genes after the HI injury
Summary
Neonatal encephalopathy due to perinatal hypoxiaischemia (HI) is a devastating disease that is a main cause of mortality in infants. The disease can lead to long-term neurological deficits, such as cerebral palsy, epilepsy, learning impairment and mental retardation. The therapeutic strategies for attenuating the injury in the clinical setting are limited. Hypothermia is established as the standard treatment, but that modality is only partially effective and has a narrow therapeutic window of 6 hours [1]. Finding new treatments to provide safe and efficient protection to neonates suffering from HI is critical. Inflammation plays a critical role in mediating brain injury induced by neonatal hypoxic-ischemic brain injury. Hypoxia-ischemia triggers inflammation minutes after the insult [2], and increasing evidence shown that post-HI is responsible for the exacerbation of the brain damage
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