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Eur J Pharm Sci ; 200: 106847, 2024 Sep 01.
Article in English | MEDLINE | ID: mdl-38972611

ABSTRACT

Exogenous insulin-like growth factor-1 (IGF-1) has been reported to promote wound healing through regulation of vascular endothelial cells (VECs). Despite the existing studies of IGF-1 on VEC and its role in angiogenesis, the mechanisms regarding anti-inflammatory and angiogenetic effects of IGF-1 remain unclear. In this study, we investigated the wound-healing process and the related signaling pathway of IGF-1 using an inflammation model induced by IFN-γ. The results demonstrated that IGF-1 can increase cell proliferation, suppress inflammation in VECs, and promote angiogenesis. In vivo studies further confirmed that IGF-1 can reduce inflammation, enhance vascular regeneration, and improve re-epithelialization and collagen deposition in acute wounds. Importantly, the Ras/PI3K/IKK/NF-κB signaling pathways was identified as the mechanisms through which IGF-1 exerts its anti-inflammatory and pro-angiogenic effects. These findings contribute to the understanding of IGF-1's role in wound healing and may have implications for the development of new wound treatment approaches.


Subject(s)
Inflammation , Insulin-Like Growth Factor I , NF-kappa B , Signal Transduction , Wound Healing , Insulin-Like Growth Factor I/metabolism , Animals , Wound Healing/drug effects , NF-kappa B/metabolism , Signal Transduction/drug effects , Inflammation/metabolism , Phosphatidylinositol 3-Kinases/metabolism , Humans , Neovascularization, Physiologic/drug effects , ras Proteins/metabolism , Male , I-kappa B Kinase/metabolism , Cell Proliferation/drug effects , Mice , Mice, Inbred C57BL , Human Umbilical Vein Endothelial Cells/drug effects , Anti-Inflammatory Agents/pharmacology , Endothelial Cells/drug effects , Endothelial Cells/metabolism , Interferon-gamma/metabolism , Interferon-gamma/pharmacology , Angiogenesis
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