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Exploring the molecular mechanism of dexmedetomidine in alleviating blood-brain barrier disruption in rats with cerebral ischemia reperfusion injury based on network pharmacology.

Overview

Authors: Xue Lv1, Wei Gao2, Zhi-Guo Zhang2, Jian-Xin Jia1,3
  1. Department of Human Anatomy, Baotou Medical College, Baotou, China
  2. Department of Anesthesiology, The Third Hospital of Baogang Group, Baotou, China
  3. Key Laboratory of Human Anatomy, Education Department of Inner Mongolia Autonomous Region, Baotou, China
Journal: Frontiers in molecular neuroscience, volume 19, article 1750882
Dates: received 20 November 2025; accepted 16 March 2026; published online 8 April 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.3389/fnmol.2026.1750882 · PMID 42027298 · PMCID PMC13099826 · OpenAlex W7152057610
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: rat (organism), stroke (population), cellular / molecular (subfield)
Methods: Statistics, Smoothing, state filtering, decompositions
Keywords: AMPK/mTOR signaling pathway, autophagy, blood–brain barrier, cerebral ischemia reperfusion injury, dexmedetomidine, network pharmacology
Topic: Neuroscience and Neuropharmacology Research (Cellular and Molecular Neuroscience, Neuroscience), according to OpenAlex
Citations: not cited yet (Europe PMC); 38 references in the paper

Abstract

Objective: This study aimed to clarify the neuroprotective effect of dexmedetomidine (DEX) against cerebral ischemia reperfusion injury (CIRI) and its underlying mechanism using network pharmacology and in vivo validation.

Methods: Network pharmacology was employed to explore the mechanism underlying DEX-mediated alleviation of CIRI. A rat CIRI model was established using the suture-occlusion method. Neurological scoring and behavioral assessments were conducted to evaluate neurological and motor functions; histological examination was performed to observe brain tissue and blood–brain barrier (BBB) injury. Western blotting and immunofluorescence analysis were utilized to assess the protein levels of factors associated with BBB integrity.

Results: Network pharmacology analysis revealed that DEX may exert a protective effect against CIRI through the AMPK/mTOR signaling pathway. DEX treatment significantly attenuated CIRI-induced impairments in neurological function and motor performance. Specifically, DEX upregulated the protein expression levels of P-AMPK/AMPK ratio, beclin 1, LC3 II/I, and ZO-1, whereas the P-mTOR/mTOR ratio and P62 were significantly downregulated, and cerebral tissue injury was alleviated.

Conclusion: DEX exerts a significant protective effect against BBB injury in rats with CIRI. This neuroprotective effect is mediated by multiple synergistic mechanisms, including the upregulation of tight junction proteins and the regulation of the AMPK/mTOR signaling pathway. Collectively, the findings of the present study suggest that DEX represents a promising potential agent for the clinical treatment of CIRI-associated BBB impairment.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

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Data

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Data availability statement

The original contributions presented in the study are publicly available. This data can be found here: https://doi.org/10.5061/dryad.q83bk3jxz.

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 29 September 2026: the first record

Recorded: type, language, journal, volume, pages, dates, 4 authors, 6 keywords, 38 references.

Cite

This paper

Lv, X., Gao, W., Zhang, Z.-G., & Jia, J.-X. (2026). Exploring the molecular mechanism of dexmedetomidine in alleviating blood-brain barrier disruption in rats with cerebral ischemia reperfusion injury based on network pharmacology. Frontiers in molecular neuroscience, 19, 1750882. https://doi.org/10.3389/fnmol.2026.1750882

BibTeX

@article{lv2026exploring,
author = {Lv, Xue and Gao, Wei and Zhang, Zhi-Guo and Jia, Jian-Xin},
title = {{Exploring the molecular mechanism of dexmedetomidine in alleviating blood-brain barrier disruption in rats with cerebral ischemia reperfusion injury based on network pharmacology}},
journal = {Frontiers in molecular neuroscience},
year = {2026},
month = apr,
volume = {19},
pages = {1750882},
publisher = {Frontiers Media SA},
issn = {1662-5099},
doi = {10.3389/fnmol.2026.1750882},
url = {https://doi.org/10.3389/fnmol.2026.1750882},
pmid = {42027298},
pmcid = {PMC13099826}
}

RIS

TY - JOUR
AU - Lv, Xue
AU - Gao, Wei
AU - Zhang, Zhi-Guo
AU - Jia, Jian-Xin
TI - Exploring the molecular mechanism of dexmedetomidine in alleviating blood-brain barrier disruption in rats with cerebral ischemia reperfusion injury based on network pharmacology
T2 - Frontiers in molecular neuroscience
J2 - Front Mol Neurosci
PY - 2026
DA - 2026/04/08
VL - 19
SP - 1750882
SN - 1662-5099
PB - Frontiers Media SA
DO - 10.3389/fnmol.2026.1750882
UR - https://doi.org/10.3389/fnmol.2026.1750882
LA - en
ER -

CSL-JSON

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