Abstract
The inflammatory process has direct effects on normal and abnormal wound healing. Hypertrophic scar formation is an aberrant form of wound healing and is an indication of an exaggerated function of fibroblasts and excess accumulation of extracellular matrix during wound healing. Two cytokines—transforming growth factor-β (TGF-β) and prostaglandin E2 (PGE2)—are lipid mediators of inflammation involving wound healing. Overproduction of TGF-β and suppression of PGE2 are found in excessive wound scarring compared with normal wound healing. Nonsteroidal anti-inflammatory drugs (NSAIDs) or their selective cyclooxygenase-2 (COX-2) inhibitors are frequently used as a pain-killer. However, both NSAIDs and COX-2 inhibitors inhibit PGE2 production, which might exacerbate excessive scar formation, especially when used during the later proliferative phase. Therefore, a balance between cytokines and medication in the pathogenesis of wound healing is needed. This report is a literature review pertaining to wound healing and is focused on TGF-β and PGE2.
Highlights
Prostaglandin (PG) E2 (PGE2), synthesized from arachidonic acid by cyclooxygenases (COX) and synthases (PGES), acts as both an inflammatory mediator and fibroblast modulator [1]
Nonsteroidal anti-inflammatory drugs (NSAIDs) or their selective cyclooxygenase-2 (COX-2) inhibitors are frequently used as a pain-killer
A better understanding of the mechanism of wound healing can be presumed from the increased number of in vitro or in vivo experiments, and a better treatment algorithm to maintain a regulated and orchestrated inflammatory response will be developed and result in effective and normal wound healing [8,9,10], most in vitro data derived from fibroblasts cultured from keloid lesions only represent the terminal stage of this disease and in vivo animal models might not present a real condition in humans
Summary
Prostaglandin (PG) E2 (PGE2), synthesized from arachidonic acid by cyclooxygenases (COX) and synthases (PGES), acts as both an inflammatory mediator and fibroblast modulator [1]. Nonsteroidal anti-inflammatory drugs (NSAIDs) or their selective cyclooxygenase-2 (COX-2) inhibitors are reported to inhibit PGE2 production and act as effective pain-killers, since they are able to reduce inflammation successfully [3, 4]. A better understanding of the mechanism of wound healing can be presumed from the increased number of in vitro or in vivo experiments, and a better treatment algorithm to maintain a regulated and orchestrated inflammatory response will be developed and result in effective and normal wound healing [8,9,10], most in vitro data derived from fibroblasts cultured from keloid lesions only represent the terminal stage of this disease and in vivo animal models might not present a real condition in humans
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