伤口愈合
姜黄素
血管生成
细胞凋亡
成纤维细胞
免疫印迹
肉芽组织
糖尿病足溃疡
流式细胞术
癌症研究
细胞生长
细胞迁移
细胞
糖尿病足
化学
医学
药理学
免疫学
糖尿病
生物化学
内分泌学
基因
体外
作者
Mengshu Cao,Zhisheng Duan,Xianting Wang,Pan Gong,Limei Zhang,Bin Ruan
标识
DOI:10.1007/s12033-023-01027-z
摘要
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.
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