Pathological scar is a common complication after wound healing. One of the most important factors that affects scar formation is inflammation. During this process, macrophages play a critical role in the wound healing process, as well as in scar formation. Notch signaling is reported to participate in inflammation and fibrosis; however, whether it affects scar formation is still unclear. In this study, RBP-J knockout mice, in which Notch signaling was down-regulated, and control mice were used, and a skin incision model was established. Sirius red staining and Masson staining suggested that RBP-J knockout could significantly reduce collagen sedimentation after wound healing. Western blot analysis and RT-PCR also confirmed the results. During wound healing, the expression of inflammatory cytokines and macrophage infiltration were decreased in RBP-J knockout mice. In vitro, it was also verified that RBP-J deficiency in macrophages effectively suppressed the expression of inflammatory cytokines and chemotaxis of macrophages after LPS stimulation. In conclusion, blocking Notch signaling in macrophages effectively alleviated scar formation by suppressing the inflammatory response and collagen sedimentation.

病理性瘢痕是伤口愈合后的常见并发症。影响疤痕形成的最重要因素之一是炎症。在此过程中，巨噬细胞在伤口愈合过程以及疤痕形成中起关键作用。据报道，Notch信号传导参与炎症和纤维化。但是，是否影响疤痕形成尚不清楚。在这项研究中，RBP-J基因敲除小鼠的Notch信号被下调，并使用了对照小鼠，并建立了皮肤切开模型。Sirius红染色和Masson染色提示RBP-J敲除可以显着减少伤口愈合后的胶原沉淀。Western blot分析和RT-PCR也证实了结果。在伤口愈合期间，在体外，还证实了巨噬细胞中RBP-J的缺乏有效抑制了LPS刺激后炎症细胞因子的表达和巨噬细胞的趋化性。总之，在巨噬细胞中阻断Notch信号传导可通过抑制炎症反应和胶原蛋白沉积而有效减轻瘢痕形成。