Sufentanil enhances the cortical neurogenesis of rats with traumatic brain injury via PI3K/AKT signal pathway

Abstract This study aimed to explore the effects of Sufentanil on the cortical neurogenesis of rats with traumatic brain injury (TBI) and investigate the potential mechanisms. Rats with TBI model were prepared and divided into sham + vehicle, TBI + vehicle, TBI + Sufentanil and TBI + Sufentanil + LY...

Full description

Saved in:
Bibliographic Details
Main Authors: Wei Gu, Mimi Wu, Ruocui Zhang, Peiyu Liu, Yang Jiao, Hui Rong
Format: Article
Language:English
Published: Nature Portfolio 2025-02-01
Series:Scientific Reports
Subjects:
Online Access:https://doi.org/10.1038/s41598-025-88344-2
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Abstract This study aimed to explore the effects of Sufentanil on the cortical neurogenesis of rats with traumatic brain injury (TBI) and investigate the potential mechanisms. Rats with TBI model were prepared and divided into sham + vehicle, TBI + vehicle, TBI + Sufentanil and TBI + Sufentanil + LY294002 (PI3K/AKT signal pathway inhibitor) four groups. The oxidative stress, inflammation, nerve cell damage, melatonin, brain-derived neurotrophic factor (BDNF), neuron regeneration and p-AKT protein level in the cortex were detected with ELISA, TUNEL, qRT-PCR, immunofluorescence and Western blot. Pain behavioral test was assessed with mechanical withdrawal threshold (MWT). The results showed Sufentanil significantly decreased the oxidative stress and inflammation levels, increased melatonin and BDNF levels, protected the nerve cells from damage, enhanced the regeneration of immature or mature neurons and the p-AKT protein expression in the cortex, and boosted MWT in TBI rats. While the rats with TBI were treated with LY294002 and Sufentanil together, the abovementioned effects of Sufentanil on the TBI rats were partially reversed. Our results indicate Sufentanil enhances the cortical neurogenesis and inhibits mechanical allodynia of rats with TBI through suppressing the oxidative stress, inflammation response and increasing the melatonin and BDNF levels partly via PI3K/AKT signal pathway.
ISSN:2045-2322