1. Academic Validation
  2. Resveratrol Improves Synaptic Plasticity in Hypoxic-Ischemic Brain Injury in Neonatal Mice via Alleviating SIRT1/NF-κB Signaling-Mediated Neuroinflammation

Resveratrol Improves Synaptic Plasticity in Hypoxic-Ischemic Brain Injury in Neonatal Mice via Alleviating SIRT1/NF-κB Signaling-Mediated Neuroinflammation

  • J Mol Neurosci. 2022 Jan;72(1):113-125. doi: 10.1007/s12031-021-01908-5.
Xin Peng  # 1 2 Jun Wang  # 3 Juan Peng 4 Hongqun Jiang 1 Kai Le 5
Affiliations

Affiliations

  • 1 Department of Otolaryngology Head and Neck Surgery, The First Affiliated Hospital of Nanchang University, No.17 Yongwaizheng Street, Nanchang, Jiangxi Province, 330006, China.
  • 2 Department of Otolaryngology, Jiangxi Province Children's Hospital, No.122 Yangming Road, Nanchang, Jiangxi Province, 330006, China.
  • 3 Department of Rehabilitation Medicine, The First Affiliated Hospital of Nanchang University, No.17 Yongwaizheng Street, Nanchang, Jiangxi Province, 330006, China.
  • 4 Department of Rehabilitation Medicine, PingXiang No.2 People's Hospital, No. 89 Pingan South Avenue, Danjiang Street, PingXiang, Jiangxi Province, 337000, China.
  • 5 Department of Rehabilitation Medicine, The First Affiliated Hospital of Nanchang University, No.17 Yongwaizheng Street, Nanchang, Jiangxi Province, 330006, China. [email protected].
  • # Contributed equally.
Abstract

Neonatal hypoxic-ischemic encephalopathy (HIE) is an obstinate disease that troubles neonatologists. At present, cognitive impairment after HIE has received increasing attention. Synaptic plasticity determines the development of cognitive function, so it is urgent to develop new drugs that can improve HIE-induced cognitive impairment. Hypoxia-ischemia (HI)-induced neuroinflammation affects synaptic plasticity. As a SIRT1 agonist, resveratrol has a powerful anti-inflammatory effect, but whether it has an effect on impaired synaptic plasticity in HIE and the potential mechanism remain unclear. In the present study, resveratrol was used to intervene in hypoxic-ischemic brain injury (HIBI) mice, and the effects on hippocampal synaptic plasticity and further mechanisms were explored through performing neurobehavioral, morphological observations, Golgi sliver staining, western blotting, and quantitative real-time polymerase chain reaction experiments. We first found that resveratrol improves HI-induced long-term cognitive and memory deficits, and then we found that resveratrol reduces hippocampal neuronal damage and increases dendritic spine density and the expression of synaptic proteins. Finally, we found that this effect may be exerted by regulating the neuroinflammatory response mediated by the SIRT1/NF-κB axis. This study provides a new theoretical basis for resveratrol to prevent long-term neurological dysfunction following HIBI.

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