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...
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Nature Portfolio
2025-02-01
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Online Access: | https://doi.org/10.1038/s41598-025-88344-2 |
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author | Wei Gu Mimi Wu Ruocui Zhang Peiyu Liu Yang Jiao Hui Rong |
author_facet | Wei Gu Mimi Wu Ruocui Zhang Peiyu Liu Yang Jiao Hui Rong |
author_sort | Wei Gu |
collection | DOAJ |
description | 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. |
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institution | Kabale University |
issn | 2045-2322 |
language | English |
publishDate | 2025-02-01 |
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spelling | doaj-art-a03a0ba1d7e64a3e80d8bbed64b12c162025-02-02T12:16:03ZengNature PortfolioScientific Reports2045-23222025-02-0115111110.1038/s41598-025-88344-2Sufentanil enhances the cortical neurogenesis of rats with traumatic brain injury via PI3K/AKT signal pathwayWei Gu0Mimi Wu1Ruocui Zhang2Peiyu Liu3Yang Jiao4Hui Rong5Department of Anesthesiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Nanjing University Medical SchoolDepartment of Anesthesiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Nanjing University Medical SchoolDepartment of Anesthesiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Nanjing University Medical SchoolDepartment of Anesthesiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Nanjing University Medical SchoolDepartment of Anesthesiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Nanjing University Medical SchoolDepartment of Anesthesiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Nanjing University Medical SchoolAbstract 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.https://doi.org/10.1038/s41598-025-88344-2SufentanilTraumatic brain injuryNeurogenesisPI3K/AKT signal pathway |
spellingShingle | Wei Gu Mimi Wu Ruocui Zhang Peiyu Liu Yang Jiao Hui Rong Sufentanil enhances the cortical neurogenesis of rats with traumatic brain injury via PI3K/AKT signal pathway Scientific Reports Sufentanil Traumatic brain injury Neurogenesis PI3K/AKT signal pathway |
title | Sufentanil enhances the cortical neurogenesis of rats with traumatic brain injury via PI3K/AKT signal pathway |
title_full | Sufentanil enhances the cortical neurogenesis of rats with traumatic brain injury via PI3K/AKT signal pathway |
title_fullStr | Sufentanil enhances the cortical neurogenesis of rats with traumatic brain injury via PI3K/AKT signal pathway |
title_full_unstemmed | Sufentanil enhances the cortical neurogenesis of rats with traumatic brain injury via PI3K/AKT signal pathway |
title_short | Sufentanil enhances the cortical neurogenesis of rats with traumatic brain injury via PI3K/AKT signal pathway |
title_sort | sufentanil enhances the cortical neurogenesis of rats with traumatic brain injury via pi3k akt signal pathway |
topic | Sufentanil Traumatic brain injury Neurogenesis PI3K/AKT signal pathway |
url | https://doi.org/10.1038/s41598-025-88344-2 |
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