Naringenin Prevents Propofol Induced Neurodegeneration in Neonatal Mice Brain and Long-Term Neurocognitive Impacts on Adults

Abstract

Background

Natural products have shown neuroprotective effects in neurodegenerative conditions. Naringenin is a natural flavonoid with various pharmacological activities especially antioxidant, anti-inflammatory and neuroprotective properties. We investigated the effects of naringenin on anesthetic propofol-induced impacts on neonatal mouse brain development and consequent long-term neurocognitive impacts during adulthood.

Materials and Methods

Female C57Bl/6 and male CD-1 mice and postnatal day 7 (P7) pups were exposed to propofol (2.5 mg/kg) and propofol with naringenin (50 mg/kg). Mice pups were allowed to grow until week 10 (adulthood), and memory and learning were assessed.

Results

Propofol caused neurodegeneration by inducing apoptosis in the neonatal mouse brains while naringenin administration prevented neuronal cell loss by preventing neuronal apoptosis in neonatal mouse brains. Propofol caused degenerative alterations in metabolic factors pH, PO ₂, glucose and lactate, which were subsequently restored by naringenin treatment. Propofol-exposed mice, when developed into adults, showed long-term neuronal deficits, impaired neurocognitive functions, and memory and learning restrictions.

Conclusion

Administration of naringenin to propofol-exposed mice resulted in significant neuroprotective effects by restoring long-term neurocognitive functions. The molecular mechanism behind the effects of naringenin was mediated by suppressing apoptosis and preventing cellular inflammation. These findings suggest that propofol administration requires careful consideration and that naringenin may prevent neurodegeneration and neurocognitive functions.