Talactoferrin Stimulates Wound Healing With Modulation of Inflammation

Engelmayer, Jose; Blezinger, Paul; Varadhachary, Atul

doi:10.1016/j.jss.2007.12.754

Cited by 54 publications

(42 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, TNF-a has potential to inhibit TGF-b and collagen gene expression in vivo (Buck et al, 1996). Furthermore, another cytokine, IL-8, is responsible for the activation of neutrophil chemotaxis which also in turn contributes to delay wound healing (Engelmayer et al, 2008). In the present study, naringin treatment suppressed the activation of NF-jB at the wound site and decreased production of pro-inflammatory cytokine mRNA levels, such as TNF-a, IL-1b, IL-6, and IL-8.…”

Section: Discussionsupporting

confidence: 55%

Wound healing potential of naringin ointment formulation via regulating the expression of inflammatory, apoptotic and growth mediators in experimental rats

Kandhare

Alam

Patil

et al. 2015

Pharmaceutical Biology

111

View full text Add to dashboard Cite

Context: Wound healing is a consequence of a complex process involving inflammatory, proliferative, and remodeling phases. Naringin, a flavanone glycoside, is associated with modulation of various oxido-inflammatory and growth factors. Aim: The aim of this study is to evaluate the wound-healing activity of naringin ointment formulation (NOF) on experimental wound models. Materials and methods: A soft paraffin-based cream containing 1, 2, and 4% (w/w) naringin was formulated and evaluated for physicochemical characters. Excision wounds and incisions wounds were used to study the topical effect of NOF for 20 d (once a day) on various biochemical, molecular, and histological parameters. Results: NOF (2 and 4%, w/w) treatment showed a significant decrease (p50.05) in wound area and epithelization period whereas the rate of wound contraction increased significantly (p50.05). The altered levels of oxido-nitrosative stress (SOD, GSH, MDA, MPO, and NO) were significantly (p50.05) restored by NOF. Treatment produced a significant increase (p50.05) in tensile strength, hydroxyproline content, and protein content. TNF-a, IL-1b, IL-6, IL-8, NF-jB, smad-7, and Bax mRNA expression were significantly down-regulated (p50.05) by NOF, whereas polymerase gamma (pol-g), smad-3, VEGF and TGF-b, and collagen-1 mRNA expressions were significantly up-regulated (p50.05) by NOF. Histological alterations in wound skin were also restored by NOF. Conclusion: NOF exerts wound healing potential via down-regulated expression of inflammatory (NF-jB, TNF-a, and ILs), apoptotic (pol-g and Bax), and up-regulated growth factor (VEGF and TGF-b) expression, thus modulating collagen-1 expression to induce angiogenesis leading to wound healing.

show abstract

Section: Discussionsupporting

confidence: 55%

Wound healing potential of naringin ointment formulation via regulating the expression of inflammatory, apoptotic and growth mediators in experimental rats

Kandhare

Alam

Patil

et al. 2015

Pharmaceutical Biology

111

View full text Add to dashboard Cite

show abstract

“…Talactoferrin-α is a recombinant form of human lactoferrin, which has been shown to have a wide range of effects on the immune system [63]. In mice, talactoferrin enhances the production of key repair inflammatory mediators IL-8, IL-6, macrophage inflammatory protein-1α, and TNF-α [64]. Although talactoferrin failed in sepsis therapy, due to its ability to control, inflammation is currently being investigated in cancer studies [65].…”

Section: Pro-and Anti-inflammatory Activitiesmentioning

confidence: 99%

Immunomodulatory effects of anti-microbial peptides

Ötvös¹

2016

Acta Microbiologica et Immunologica Hungarica

View full text Add to dashboard Cite

Anti-microbial peptides (AMPs) were originally thought to exert protecting actions against bacterial infection by disintegrating bacterial membranes. Upon identification of internal bacterial targets, the view changed and moved toward inhibition of prokaryote-specific biochemical processes. However, the level of none of these activities can explain the robust efficacy of some of these peptides in animal models of systemic and cutaneous infections. A rapidly growing panel of reports suggests that AMPs, now called host-defense peptides (HDPs), act through activating the immune system of the host. This includes recruitment and activation of macrophages and mast cells, inducing chemokine production and altering NF-κB signaling processes. As a result, both pro-and anti-inflammatory responses are elevated together with activation of innate and adaptive immunity mechanisms, wound healing, and apoptosis. HDPs sterilize the systemic circulation and local injury sites significantly more efficiently than pure single-endpoint in vitro microbiological or biochemical data would suggest and actively aid recovering from tissue damage after or even without bacterial infections. However, the multiple and, often opposing, immunomodulatory functions of HDPs require exceptional care in therapeutic considerations.

show abstract

“…Indeed, the application of talactoferrin to wounded diabetic and nondiabetic mice modulated the early inflammatory response with evidence of increased CXCL8 expression associated with improved wound closure. 131 Furthermore, improved healing has been demonstrated in diabetic ulcers with the application of a talactoferrin gel in humans. 132 A consistent finding in pressure ulcers, the diabetic foot and venous stasis ulcers is an accumulation of senescent fibroblasts.…”

Section: 117mentioning

confidence: 99%