THE ROLE OF CELECOXIB-MEDIATED COX-2 INHIBITION IN MODULATING NEUROINFLAMMATION IN HUMANS: A REVIEW

Obioma R. Emeka-Obi; Chekwube A. Ezegbe; Ezinne C. Okorafor; Chikaodi G. Onuaja; Nkesi A. Amadi; Ruhuoma G. Amadi

doi:10.22270/ujpr.v11i4.1577

Obioma R. Emeka-Obi Department of Haematology, School of Basic Clinical Sciences, College of Medicine, Federal University of Technology, Owerri, Imo State, Nigeria.
Chekwube A. Ezegbe Department of Pharmaceutical Technology and Industrial Pharmacy, University of Nigeria, Nsukka, Nigeria.
Ezinne C. Okorafor Department of Pharmacology, School of Basic Clinical Sciences, College of Medicine, Federal University of Technology, Owerri, Imo State, Nigeria
Chikaodi G. Onuaja Department of Environmental Science and Resource Management, National Open University of Nigeria, Abuja, Nigeria.
Nkesi A. Amadi Centre for Occupational Health and Safety, University of Port-Harcourt, Choba, Rivers State, Nigeria.
Ruhuoma G. Amadi University of Regina, 3737, Wascana Parkway, Regina Saskatchewan S4S0A2, Canada.

10.22270/ujpr.v11i4.1577

Keywords:

Celecoxib, COX-2 inhibitor, macrophage, neuroinflammation, peripheral nerve regeneration, polarization, prostaglandin E2, Schwann cells

Abstract

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.