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.
摘要：
已报道外源性胰岛素样生长因子-1(IGF-1)通过调节血管内皮细胞(VEC)促进伤口愈合。尽管已有IGF-1对VEC的作用及其在血管生成中的作用的研究,关于IGF-1的抗炎和血管生成作用的机制尚不清楚.在这项研究中,我们使用IFN-γ诱导的炎症模型研究了IGF-1的伤口愈合过程和相关信号通路。结果证明IGF-1能促进细胞增殖,抑制VECs中的炎症，促进血管生成。体内研究进一步证实，IGF-1可以减轻炎症，增强血管再生，并改善急性伤口的再上皮化和胶原沉积。重要的是,Ras/PI3K/IKK/NF-κB信号通路被确定为IGF-1发挥其抗炎和促血管生成作用的机制。这些发现有助于理解IGF-1在伤口愈合中的作用，并可能对开发新的伤口治疗方法有意义。
