Wnt-3a improves functional recovery after spinal cord injury by regulating the inflammatory and apoptotic response in rats via wnt/β-catenin signaling pathway.

Apoptosis Inflammation Spinal cord injury Wnt-3a Wnt/β-catenin signaling pathway

Journal

Brain research
ISSN: 1872-6240
Titre abrégé: Brain Res
Pays: Netherlands
ID NLM: 0045503

Informations de publication

Date de publication:
01 Jan 2024
Historique:
received: 06 06 2023
revised: 29 09 2023
accepted: 16 10 2023
pubmed: 20 10 2023
medline: 20 10 2023
entrez: 20 10 2023
Statut: ppublish

Résumé

The specific molecular mechanism of neuroprotective effects of wnt-3a on spinal cord injury (SCI) has not been elucidated. In our study, we evaluated the recovery of motor function after SCI by BBB, observed neuronal apoptosis by western blot and TUNEL, observed the changes of neuronal inflammation by western blot and immunofluorescence staining, and observed the changes of motoneurons and spinal cord area in the anterior horn of the spinal cord via Nissl and HE staining. We found that wnt-3a could significantly promote the recovery of motor function, reduce the loss of motor neurons in the anterior horn of the spinal cord, promote the recovery of injured spinal cord tissue, inhibit neuronal apoptosis and inflammatory response, and ultimately promote neuronal function after SCI. However, when XAV939 inhibits the wnt/β-catenin signaling pathway, the neuroprotective effects of wnt-3a are also significantly inhibited. The above results together indicated that wnt-3a exerts its neuroprotective effect on after SCI via activating the wnt/β-catenin signaling pathway.

Identifiants

pubmed: 37858855
pii: S0006-8993(23)00408-0
doi: 10.1016/j.brainres.2023.148637
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

148637

Informations de copyright

Copyright © 2023. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Kai Gao (K)

Postdoctoral of Shandong University of Traditional Chinese Medicine, Jinan, China; Department of Orthopedics, Jining No.1 People's Hospital, Jining, China.

Wenbo Shao (W)

Department of Orthopedics, Jining No.2 People's Hospital, Jining, China.

Tian Wei (T)

School of Clinical Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China.

Zihan Yan (Z)

School of Clinical Medicine, Jining Medical University, Jining, China.

Nianhu Li (N)

Postdoctoral of Shandong University of Traditional Chinese Medicine, Jinan, China; Department of Orthopedics, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, China. Electronic address: tigerlee073@126.com.

Chaoliang Lv (C)

Department of Orthopedics, Jining No.1 People's Hospital, Jining, China; School of Clinical Medicine, Jining Medical University, Jining, China. Electronic address: lvchaolianggk@163.com.

Classifications MeSH