Silencing miR-155-5p alleviates hippocampal damage in kainic acid-induced epileptic rats via the Dusp14/MAPK pathway.

Autor: Fang Q; Department of Pediatrics, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian 350001, China. Electronic address: tiantian3618@163.com., Cai Y; Department of Pediatrics, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian 350001, China., Chi J; Department of Pediatrics, Ningde Normal University, NingDe, Ningde, Fujian 352000, China., Yang Y; Department of Pediatrics, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian 350001, China., Chen Q; Department of Pediatrics, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian 350001, China. Electronic address: Chenqiaobin1973@sohu.com., Chen L; Department of Pediatrics, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian 350001, China., Zhang J; Shengli Clinical Medical College of Fujian Medical University, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian 350001, China; Department of Emergency, Fujian Provincial Hospital, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian 350001, China; Fujian Provincial Key Laboratory of Emergency Medicine, Fuzhou, Fujian 350001, China., Ke J; Shengli Clinical Medical College of Fujian Medical University, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian 350001, China; Department of Emergency, Fujian Provincial Hospital, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian 350001, China; Fujian Provincial Key Laboratory of Emergency Medicine, Fuzhou, Fujian 350001, China., Wu Y; Department of Pediatrics, Ningde Maternal and Child Health Hospital, Ningde, Fujian 352000, China., He X; Department of Pediatrics, Fuzhou First General Hospital with Fujian Medical University, Fuzhou, Fujian 350001, China.
Jazyk: angličtina
Zdroj: Brain research bulletin [Brain Res Bull] 2024 Oct 15; Vol. 217, pp. 111057. Date of Electronic Publication: 2024 Aug 28.
DOI: 10.1016/j.brainresbull.2024.111057
Abstrakt: Epilepsy with recurrent seizures is characterized by neuronal damage and glial proliferation induced by brain inflammation. Recurrent seizures can lead to changes in the microRNA (miRNA) spectrum, significantly influencing the inflammatory response of microglia. MiR-155-5p, as a pro-inflammatory miRNA, is increased in the epileptic brain. However, its specific role in acute seizures remains unknown. The study aimed to develop a new strategy for treating epilepsy by investigating how silencing of miR-155-5p initiated its anticonvulsive mechanism. The level of miR-155-5p was up-regulated in the hippocampus of epileptic immature rats induced by kainic acid (KA). The use of antago-miR-155-5p exerted significant beneficial effects on the seizure scores, brain discharges and cognition in immature rats following KA-induced epilepsy. Antago-miR-155-5p also inhibited neuron damage and microglial activation. Moreover, the silencing of miR-155-5p significantly inhibited the Dual-specificity phosphatase 14 (Dusp14)/ mitogen-activated protein kinase (MAPK) axis in vivo. MiR-155-5p interacted with dusp14 to regulate MAPK signaling way expression, verified by a dual-luciferase reporter assay. The results suggested that the silencing of miR-155-5p might reduce hippocampal damage in epileptic immature rats induced by KA via Dusp14/MAPK signaling way. This implied that miR-155-5p could serve as a therapeutic tool to prevent the development of epilepsy.
Competing Interests: Declaration of Competing Interest The authors declare that there are no conflicts of interest associated with this manuscript
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE