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ISSN: 2157-7099

Journal of Cytology & Histology
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  • Research Article   
  • J Cytol Histol 2017, Vol 8(5): 481
  • DOI: 10.4172/2157-7099.1000481

Inhibition of Wound TGF Beta-1 by Celecoxib: A Possible Therapeutic Route for Scar Free Wound

Seham Abd El-Raouf Abd El-Aleem1* and Edward Jude2
1Department of Histology, Minia Faculty of Medicine, , UK
2Tameside Hospital NHS Foundation Trust and the University of Manchester, , UK
*Corresponding Author : Seham Abd El-Raouf Abd El-Aleem, Department of Histology, Minia Faculty of Medicine, Tameside Hospital NHS Foundation Trust University and University of Manchester, UK, Tel: 0020102997270, Email: [email protected]

Received Date: Oct 01, 2017 / Accepted Date: Oct 25, 2017 / Published Date: Nov 03, 2017

Abstract

Background: Wound healing is a highly ordered dynamic process associated with inflammation at early stages and with permanent scarring at late stages. Scars could be disfiguring and could advance to be hypertrophic or keloid scars, this would have a strong physical and psychological impact on the patients afterward. The role of inflammatory mediators which could be pro- or anti-inflammatory, pro-or antifibrotic was the focus of wound healing research for decades and the balance between them is the key factor determining the outcome of healing.
Aims: In this study, we investigate the correlation and the interrelation between the pro-inflammatory Cyclooxygenase-2 (COX-2) and the pro fibrotic (TGF-Beta-1) in an in vivo model of incisional dermal wound healing and the effect of a selective COX-2 inhibiton the progression of repair and scar formation.
Materials and methods: Adult male Sprague-Dawley rats received four full thickness dermal wounds. a selective COX-2 inhibitor was applied to the wounds immediately postwounding twice daily for two days. Wounds and scars were then harvested and at different time points and processed for COX-2 and TGF Beta-1 immunostaining and for collagen staining. Immunoreactivity was semi quantified using Image J.
Results: We have shown upregulation of COX-2, co-upregulation and colocalization of TGF-Beta-1 and COX-2 two days postwounding during the inflammatory phase. Celecoxib application significantly inhibited both COX- 2 (P<0.01) and TGF Beta-1 (P<0.001). It improved wound healing microscopically and macroscopically, through reducing inflammatory cell infiltrate, granulation tissues formation and early closure of the incision. Additionally, there was marked improvement in the postwounding scarring. There was a significantly (P<0.01) correlation between COX-2 and TGF Beta-1 (Pearson Correlation=0.94).
Conclusion: The overall effect of COX-2 inhibitor was shortening of the inflammatory phase of wound healing with subsequent minimization of the associated tissue destruction and consequently improvement of the scar quality. COX-2 inhibitors regulate inflammatory phase of the wound. They could regulate collagen deposition by
regulating the produc-tion of the pro fibrotic TGF Beta-1 production, through autocrine/paracrine effect. Therefore, early application of COX-2 inhibitors to wounds immediately after injury/surgery could enhance the repair and improve the quality of scar.

Keywords: Wound healing; Cyclooxygenase; TGF beta; Scar; Fibrosis; Celecoxib

Citation: Abd El-Aleem SAER, Jude E (2017) Inhibition of Wound TGF Beta-1 by Celecoxib: A Possible Therapeutic Route for Scar Free Wound. J Cytol Histol 8: 481. Doi: 10.4172/2157-7099.1000481

Copyright: © 2017 Abd El-Aleem SAER, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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