The skin plays an important role in protecting the body from mechanical damage, microbial infection, ultraviolet radiation, and extreme temperatures. Many products as well as ongoing studies have focused on skin injury and repair; however, unlimited challenges are still being faced. Furthermore, the drugs that are currently on the market are not adequate to meet the increasing medical needs. This study aimed to discover whether our new product can efficiently promote wound repair and skin restoration.
ĩn this study, we applied a new AIMP1-derived peptide (AdP), NeoPep S, administered in two dose types (1 ppm and 3 ppm), and determined their effect on skin wound repair in rat models. Cell proliferation and inflammatory responses were assessed using immunofluorescence (IF) staining and ELISA assay.
As expected, our results showed more rapid and satisfactory progress in wound closure upon treatment with NeoPep S 3 ppm than with NeoPep S 1 ppm. The 3 ppm peptide derived from AIMP1 protein, harmoniously interacted with the wound to promote re-epithelialization and collagen regeneration, as well as the down-regulation of several types of cytokines and chemokines, such as TNF-α, IL-6, IL-8, IL-lβ, MCP-1, and F4/80. Moreover, it was demonstrated to promote fibroblast proliferation, migration, and differentiation by TGF-βl and TGF-β3 modulation, as well as nitrite and reactive oxygen species scavenging.
The novel peptide NeoPep S 3 ppm showed high effectiveness and safety in wound healing.
Copyright © 2022, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Mineralocorticoid receptor (MR) blockade reduces morbidity and mortality after acute myocardial infarction; however, the underlying mechanisms are still under investigation. This study examined whether MR antagonism promotes healing of the infarcted myocardium. Starting immediately after coronary ligation, male Wistar rats were treated with the selective MR antagonist eplerenone (100 mg/kg per day by gavage) or placebo for 2 to 7 days. At 7 days, eplerenone therapy versus placebo significantly reduced thinning and dilatation of the infarcted wall, improved left ventricular function, and enhanced neovessel formation in the injured myocardium. At 2 days, eplerenone-treated rats displayed lower plasma corticosterone levels, higher circulating blood monocytes, and more macrophages infiltrating the infarcted myocardium. MR blockade led to a transient upregulation (at days 2 and 3 but not at day 7) of monocyte chemoattractant protein-1, tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, interleukin-10, and interleukin-4 and an increase in factor XIIIa protein expression in the healing myocardium. Prevention of macrophage accumulation into the infarct zone by treatment with liposome-encapsulated clodronate almost abrogated the protein expression of factor XIIIa and the beneficial effects of eplerenone on infarct expansion. In conclusion, selective MR blockade immediately after myocardial infarction accelerated macrophage infiltration and transiently increased the expression of healing promoting cytokines and factor XIIIa in the injured myocardium resulting in enhanced infarct neovascularization and reduced early LV dilation and dysfunction.