PDF(Pubmed)
Abstract：
UNASSIGNED: One of the key obstacles to the healing of diabetic wound is the persistence of active inflammation. We previously demonstrated the potential of cell-free fat extract (CEFFE) to promote the healing of diabetic wounds, and annexin A5 (A5) is a crucial anti-inflammatory protein within CEFFE. This study aimed to evaluate the therapeutic potential of A5 in diabetic wounds.
UNASSIGNED: A5 was loaded into GelMA hydrogels and applied to skin wounds of diabetic mice in vivo. The diabetic wounds with the treatment of GelMA-A5 were observed for 14 days and evaluated by histological analysis. Accessment of inflammation regulation were conducted through anti-CD68 staining, anti-CD86 and anti-CD206 staining, and qRT-PCR of wound tissue. In presence of A5, macrophages stimulated by lipopolysaccharide (LPS) in vitro, and detected through qRT-PCR, flow cytometry, and immunocytofluorescence staining. Besides, epithelial cells were co-cultured with A5 for epithelialization regulation by CCK-8 assay and cell migration assay.
UNASSIGNED: A5 could promote diabetic wound healing and regulate inflammations by promoting the transition of macrophages from M1 to M2 phenotype. In vitro experiments demonstrated that A5 exerted a significant effect on reducing pro-inflammatory factors and inhibiting the polarization of macrophages from M0 toward M1 phenotype. A5 significantly promoted the migration of epithelial cells.
UNASSIGNED: Annexin A5 has a significant impact on the regulation of macrophage inflammation and promotion of epithelialization.
UNASSIGNED: A5 was loaded into GelMA hydrogels and applied to skin wounds of diabetic mice in vivo. The diabetic wounds with the treatment of GelMA-A5 were observed for 14 days and evaluated by histological analysis. Accessment of inflammation regulation were conducted through anti-CD68 staining, anti-CD86 and anti-CD206 staining, and qRT-PCR of wound tissue. In presence of A5, macrophages stimulated by lipopolysaccharide (LPS) in vitro, and detected through qRT-PCR, flow cytometry, and immunocytofluorescence staining. Besides, epithelial cells were co-cultured with A5 for epithelialization regulation by CCK-8 assay and cell migration assay.
UNASSIGNED: A5 could promote diabetic wound healing and regulate inflammations by promoting the transition of macrophages from M1 to M2 phenotype. In vitro experiments demonstrated that A5 exerted a significant effect on reducing pro-inflammatory factors and inhibiting the polarization of macrophages from M0 toward M1 phenotype. A5 significantly promoted the migration of epithelial cells.
UNASSIGNED: Annexin A5 has a significant impact on the regulation of macrophage inflammation and promotion of epithelialization.
摘要：
■糖尿病伤口愈合的关键障碍之一是活动性炎症的持续存在。我们先前证明了无细胞脂肪提取物（CEFFE）促进糖尿病伤口愈合的潜力，膜联蛋白A5（A5）是CEFFE中至关重要的抗炎蛋白。本研究旨在评估A5在糖尿病伤口中的治疗潜力。
■将A5加载到GelMA水凝胶中,并在体内应用于糖尿病小鼠的皮肤伤口。用GelMA-A5处理的糖尿病伤口观察14天并通过组织学分析进行评估。通过抗CD68染色进行炎症调节，抗CD86和抗CD206染色，和伤口组织的qRT-PCR。在A5的存在下，脂多糖（LPS）在体外刺激的巨噬细胞，并通过qRT-PCR检测，流式细胞术,和免疫荧光染色。此外,上皮细胞与A5共培养，通过CCK-8测定和细胞迁移测定进行上皮化调节。
■A5可能通过促进巨噬细胞从M1表型向M2表型转变来促进糖尿病创面愈合和调节炎症。体外实验表明，A5对降低促炎因子和抑制巨噬细胞从M0向M1表型的极化具有显著作用。A5明显增进了上皮细胞的迁徙。
■膜联蛋白A5对调节巨噬细胞炎症和促进上皮化具有显着影响。
■将A5加载到GelMA水凝胶中,并在体内应用于糖尿病小鼠的皮肤伤口。用GelMA-A5处理的糖尿病伤口观察14天并通过组织学分析进行评估。通过抗CD68染色进行炎症调节，抗CD86和抗CD206染色，和伤口组织的qRT-PCR。在A5的存在下，脂多糖（LPS）在体外刺激的巨噬细胞，并通过qRT-PCR检测，流式细胞术,和免疫荧光染色。此外,上皮细胞与A5共培养，通过CCK-8测定和细胞迁移测定进行上皮化调节。
■A5可能通过促进巨噬细胞从M1表型向M2表型转变来促进糖尿病创面愈合和调节炎症。体外实验表明，A5对降低促炎因子和抑制巨噬细胞从M0向M1表型的极化具有显著作用。A5明显增进了上皮细胞的迁徙。
■膜联蛋白A5对调节巨噬细胞炎症和促进上皮化具有显着影响。
