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    <doi_batch_id>_1789449467</doi_batch_id>
    <timestamp>20260915131747000</timestamp>
    <depositor>
      <depositor_name>Editor</depositor_name>
      <email_address>editor.jddt@gmail.com</email_address>
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    <registrant>Universal Journal of Pharmaceutical Research</registrant>
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      <journal_metadata>
        <full_title>Universal Journal of Pharmaceutical Research</full_title>
        <abbrev_title>Univ J Pharm Res</abbrev_title>
        <issn media_type="electronic">2456-8058</issn>
        <issn media_type="print">2831-5235</issn>
      </journal_metadata>
      <journal_issue>
        <publication_date media_type="online">
          <month>09</month>
          <day>15</day>
          <year>2026</year>
        </publication_date>
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        <titles>
          <title>THE ROLE OF CELECOXIB-MEDIATED COX-2 INHIBITION IN MODULATING NEUROINFLAMMATION IN HUMANS: A REVIEW</title>
        </titles>
        <contributors>
          <person_name contributor_role="author" sequence="first">
            <surname>Obioma R. Emeka-Obi</surname>
          </person_name>
          <person_name contributor_role="author" sequence="additional">
            <surname>Chekwube A. Ezegbe</surname>
          </person_name>
          <person_name contributor_role="author" sequence="additional">
            <surname>Ezinne C. Okorafor</surname>
          </person_name>
          <person_name contributor_role="author" sequence="additional">
            <surname>Chikaodi G. Onuaja</surname>
          </person_name>
          <person_name contributor_role="author" sequence="additional">
            <surname>Nkesi A. Amadi</surname>
          </person_name>
          <person_name contributor_role="author" sequence="additional">
            <surname>Ruhuoma G. Amadi</surname>
          </person_name>
        </contributors>
        <jats:abstract xmlns:jats="http://www.ncbi.nlm.nih.gov/JATS1">
          <jats:p>Peripheral nerve injury triggers a complex cascade of neuroinflammatory events that are essential for initiating regeneration but can become detrimental when prolonged. Cyclooxygenase-2 (COX-2) and its primary product prostaglandin E2 (PGE2) are rapidly upregulated at the injury site by Schwann cells, macrophages, and neurons. While early PGE2 signaling promotes Schwann cell dedifferentiation, cytokine release and axonal sprouting, sustained COX-2 activity contributes to chronic neuroinflammation, neuropathic pain, and glial scar formation that physically and chemically inhibit axonal regrowth. Celecoxib, a selective COX-2 inhibitor, has emerged as a pharmacological tool to modulate this dual role of neuroinflammation during peripheral nerve repair.  This review synthesizes current evidence on the mechanisms by which celecoxib-mediated COX-2 inhibition influences the regenerative microenvironment. Future research should prioritize dose-dependent studies, injury-stage-specific administration, and biomaterial-based delivery to maximize regenerative benefits while minimizing adverse effects on nerve repair. Understanding the precise interplay between COX-2, PGE2, and downstream regenerative pathways will be the keys to translating celecoxib based therapies into clinical applications for peripheral neuropathies and traumatic nerve injuries.
                      
Peer Review History: 
Received 5 June 2026;   Reviewed 8 July 2026; Accepted  6 August; Available online 15 September 2026
Academic Editor: Dr. Ali Abdullah Al-yahawi, Al-Razi university, Department of Pharmacy, Yemen, alyahawipharm@yahoo.com
Reviewers:
Dr. Kingsley C Anukam, University of Benin, Nigeria, kanukam@gmail.com
Dr. Liliya Logoyda, Horbachevsky Ternopil State Medical University, Ukraine, logojda@tdmu.edu.ua</jats:p>
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          <month>09</month>
          <day>15</day>
          <year>2026</year>
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          <doi>10.22270/ujpr.v11i4.1577</doi>
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