Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling Pathway

To investigate the mechanism dexmedetomidine in relieving the neurotoxicity of a developing brain induced by sevoflurane. Sprague-Dawley rats, 6 days old, were randomly divided into three groups. Rats in the control group were inhaled with air after injection of normal saline; rats in the sevofluran...

Full description

Saved in:
Bibliographic Details
Main Authors: Yunxia Dong, Wei Hong, Zhiyin Tang, Yan Gao, Xiuying Wu, Hongtao Liu
Format: Article
Language:English
Published: Wiley 2020-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2020/5458061
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850158716503982080
author Yunxia Dong
Wei Hong
Zhiyin Tang
Yan Gao
Xiuying Wu
Hongtao Liu
author_facet Yunxia Dong
Wei Hong
Zhiyin Tang
Yan Gao
Xiuying Wu
Hongtao Liu
author_sort Yunxia Dong
collection DOAJ
description To investigate the mechanism dexmedetomidine in relieving the neurotoxicity of a developing brain induced by sevoflurane. Sprague-Dawley rats, 6 days old, were randomly divided into three groups. Rats in the control group were inhaled with air after injection of normal saline; rats in the sevoflurane group were injected with normal saline and inhaled with 3% sevoflurane for 2 h in three consecutive day; rats in the dexmedetomidine group were inhaled with 3% sevoflurane after intraperitoneal injection of dexmedetomidine 25 μg/kg. WB results showed that mBDNF, pTrkB/TrkB, and CREB were significantly decreased in the hippocampus of the sevoflurane group, which are significantly upregulated in the dexmedetomidine group. In the sevoflurane group, proBDNF, P75NRT, and RhoA were significantly increased, which were significantly lower than those in the dexmedetomidine group than those in the sevoflurane group. The expression BDNF was downregulated in the sevoflurane group, while the proBDNF was upregulated in the sevoflurane group. In the Morris water maze test, the escape latency of the sevoflurane group was significantly prolonged. In sevoflurane groups, the number of crossing platform was significantly reduced, the synaptic protein decreased significantly, and this effect was reversed in rats of the dexmedetomidine group. Dexmedetomidine could reduce synaptic plasticity decline in developing rats induced by sevoflurane, through downregulating the proBDNF-p75NTR-RhoA pathway and upregulating BDNF-TrkB-CREB.
format Article
id doaj-art-660038df724948c890504686ff45c19a
institution OA Journals
issn 0962-9351
1466-1861
language English
publishDate 2020-01-01
publisher Wiley
record_format Article
series Mediators of Inflammation
spelling doaj-art-660038df724948c890504686ff45c19a2025-08-20T02:23:48ZengWileyMediators of Inflammation0962-93511466-18612020-01-01202010.1155/2020/54580615458061Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling PathwayYunxia Dong0Wei Hong1Zhiyin Tang2Yan Gao3Xiuying Wu4Hongtao Liu5Department of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, ChinaDepartment of Ultrasound, The Third Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang, ChinaDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, ChinaDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, ChinaDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, ChinaDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, ChinaTo investigate the mechanism dexmedetomidine in relieving the neurotoxicity of a developing brain induced by sevoflurane. Sprague-Dawley rats, 6 days old, were randomly divided into three groups. Rats in the control group were inhaled with air after injection of normal saline; rats in the sevoflurane group were injected with normal saline and inhaled with 3% sevoflurane for 2 h in three consecutive day; rats in the dexmedetomidine group were inhaled with 3% sevoflurane after intraperitoneal injection of dexmedetomidine 25 μg/kg. WB results showed that mBDNF, pTrkB/TrkB, and CREB were significantly decreased in the hippocampus of the sevoflurane group, which are significantly upregulated in the dexmedetomidine group. In the sevoflurane group, proBDNF, P75NRT, and RhoA were significantly increased, which were significantly lower than those in the dexmedetomidine group than those in the sevoflurane group. The expression BDNF was downregulated in the sevoflurane group, while the proBDNF was upregulated in the sevoflurane group. In the Morris water maze test, the escape latency of the sevoflurane group was significantly prolonged. In sevoflurane groups, the number of crossing platform was significantly reduced, the synaptic protein decreased significantly, and this effect was reversed in rats of the dexmedetomidine group. Dexmedetomidine could reduce synaptic plasticity decline in developing rats induced by sevoflurane, through downregulating the proBDNF-p75NTR-RhoA pathway and upregulating BDNF-TrkB-CREB.http://dx.doi.org/10.1155/2020/5458061
spellingShingle Yunxia Dong
Wei Hong
Zhiyin Tang
Yan Gao
Xiuying Wu
Hongtao Liu
Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling Pathway
Mediators of Inflammation
title Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling Pathway
title_full Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling Pathway
title_fullStr Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling Pathway
title_full_unstemmed Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling Pathway
title_short Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling Pathway
title_sort dexmedetomidine attenuates neurotoxicity in developing rats induced by sevoflurane through upregulating bdnf trkb creb and downregulating probdnf p75nrt rhoa signaling pathway
url http://dx.doi.org/10.1155/2020/5458061
work_keys_str_mv AT yunxiadong dexmedetomidineattenuatesneurotoxicityindevelopingratsinducedbysevofluranethroughupregulatingbdnftrkbcrebanddownregulatingprobdnfp75nrtrhoasignalingpathway
AT weihong dexmedetomidineattenuatesneurotoxicityindevelopingratsinducedbysevofluranethroughupregulatingbdnftrkbcrebanddownregulatingprobdnfp75nrtrhoasignalingpathway
AT zhiyintang dexmedetomidineattenuatesneurotoxicityindevelopingratsinducedbysevofluranethroughupregulatingbdnftrkbcrebanddownregulatingprobdnfp75nrtrhoasignalingpathway
AT yangao dexmedetomidineattenuatesneurotoxicityindevelopingratsinducedbysevofluranethroughupregulatingbdnftrkbcrebanddownregulatingprobdnfp75nrtrhoasignalingpathway
AT xiuyingwu dexmedetomidineattenuatesneurotoxicityindevelopingratsinducedbysevofluranethroughupregulatingbdnftrkbcrebanddownregulatingprobdnfp75nrtrhoasignalingpathway
AT hongtaoliu dexmedetomidineattenuatesneurotoxicityindevelopingratsinducedbysevofluranethroughupregulatingbdnftrkbcrebanddownregulatingprobdnfp75nrtrhoasignalingpathway