PDF(Pubmed)
Abstract：
The objective of this study was to investigate the mechanism of curcumin in diabetic foot ulcer (DFU) wound healing. A DFU rat model was established, and fibroblasts were cultured in a high-glucose (HG) environment to create a cell model. Various techniques, including Western blot, RT‒qPCR, flow cytometry, Transwell, cell scratch test and H&E staining, were employed to measure the levels of relevant genes and proteins, as well as to assess cell proliferation, apoptosis, migration, and pathological changes. The results showed that miR-152-3p was overexpressed in DFU patients, while FBN1 was underexpressed. Curcumin was found to inhibit fibroblast apoptosis, promote proliferation, migration, and angiogenesis in DFU rats, and accelerate wound healing in DFU rats. In addition, overexpression of miR-152-3p weakened the therapeutic effect of curcumin, while overexpression of FBN1 reversed the effects of the miR-152-3p mimic. Further investigations into the underlying mechanisms revealed that curcumin expedited wound healing in DFU rats by restoring the FBN1/TGF-β pathway through the inhibition of miR-152-3p. In conclusion, curcumin can suppress the activity of miR-152-3p, which, in turn, leads to the rejuvenation of the FBN1/TGF-β pathway and accelerates DFU wound healing.
摘要：
目的探讨姜黄素对糖尿病足溃疡(DFU)创面愈合的作用机制。建立DFU大鼠模型,和成纤维细胞在高葡萄糖（HG）环境中培养以创建细胞模型。各种技术,包括蛋白质印迹,RT-qPCR,流式细胞术,Transwell,细胞划痕试验和H&E染色,被用来测量相关基因和蛋白质的水平，以及评估细胞增殖，凋亡，迁移,和病理变化。结果显示miR-152-3p在DFU患者中过度表达,而FBN1的压力不足。发现姜黄素抑制成纤维细胞凋亡，促进扩散,迁移,DFU大鼠的血管生成，并加速DFU大鼠的伤口愈合。此外,miR-152-3p的过表达削弱了姜黄素的治疗作用，而FBN1的过表达逆转了miR-152-3p模拟物的作用。对潜在机制的进一步研究表明，姜黄素通过抑制miR-152-3p恢复FBN1/TGF-β途径来加速DFU大鼠的伤口愈合。总之,姜黄素可以抑制miR-152-3p的活性，which,反过来,导致FBN1/TGF-β途径的恢复并加速DFU伤口愈合。
