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ORIGINAL RESEARCH article

Front. Pharmacol.
Sec. Neuropharmacology
Volume 15 - 2024 | doi: 10.3389/fphar.2024.1437445

Effect of Dexmedetomidine on ncRNA and mRNA Profiles of Cerebral Ischemia-Reperfusion Injury in Transient Middle Cerebral Artery Occlusion Rats Model

Provisionally accepted
Zhen Zhen Zhang Zhen Zhen Zhang *Abdul Nasir Abdul Nasir Dong Li Dong Li *Qian Bai Qian Bai *Feng Yuan Feng Yuan *
  • Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China

The final, formatted version of the article will be published soon.

    Ischemic stroke poses a significant global health burden, with rapid revascularization treatments being crucial but often insufficient to mitigate ischemia-reperfusion (I/R) injury. Dexmedetomidine (DEX) has shown promise in reducing cerebral I/R injury, but its potential molecular mechanism, particularly its interaction with non-coding RNAs (ncRNAs), remains unclear. This study investigates DEX's therapeutic effect and potential molecular mechanisms in reducing cerebral I/R injury. A transient middle cerebral artery obstruction (tMACO) model was established to simulate cerebral I/R injury in adult rats. DEX was administered pre-ischemia and post-reperfusion. RNA sequencing and bioinformatic analyses were performed on the ischemic cerebral cortex to identify differentially expressed non-coding RNAs (ncRNAs) and mRNAs. The sequencing results showed 6494 differentially expressed (DE) mRNA and 2698 DE circRNA between the sham (S) and tMCAO (I/R) groups. Additionally, 1809 DE lncRNA, 763 DE mRNA, and 2795 DE circRNA were identified between the I/R group and tMCAO+DEX (I/R+DEX) groups. Gene ontology (GO) analysis indicated significant enrichment in multicellular biogenesis, plasma membrane components, and protein binding. KEGG analysis further highlighted the potential mechanism of DEX action in reducing cerebral I/R injury, with hub genes involved in inflammatory pathways. This study demonstrates DEX's efficacy in reducing cerebral I/R injury and offers insights into its brain-protective effects, especially in ischemic stroke. Further research is warranted to fully understand DEX's neuroprotective mechanisms and its clinical applications.

    Keywords: ischemia-reperfusion injury, Dexmedetomidine, Transcriptomics, non-coding RNAs, ischemic stroke

    Received: 23 May 2024; Accepted: 18 Jul 2024.

    Copyright: © 2024 Zhen Zhang, Nasir, Li, Bai and Yuan. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Zhen Zhen Zhang, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China
    Dong Li, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China
    Qian Bai, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China
    Feng Yuan, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.