Molecular biology reports · 2025
Upregulation of miR-155-5p impaired ginsenoside Rg1-mediated wound healing in diabetic foot ulcers by targeting E2F2/CDCA7L signaling : Rg1 improves DFU wound healing via inhibiting miR-155-5p.
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Xiao Meimei, Qiu Yue, Jiang Cancai, Zhang Chenhao, Yao Jun
Аннотация
BACKGROUND: Numerous studies have confirmed that ginsenoside Rg1 can promote wound healing in diabetic foot ulcers (DFU), yet the underlying mechanisms remain unclear. This study aimed to investigate the function of miR-155 in Rg1-mediated DFU wound healing and its regulatory mechanism.
METHODS: A DFU mouse model was established, and wound healing was assessed using macroscopic observation and HE staining. The oxidative stress level was evaluated by ELISA and immunohistochemistry assays. In vitro, ELISA, RT-qPCR, CCK-8, transwell migration, and tube formation assays were used to evaluate oxidative stress, wound closure, and angiogenesis in high glucose (HG)-induced HUVECs, respectively. Dual luciferase-reporter assay determined the interaction between miR-155-5p and E2F2.
RESULTS: Here, we observed that Rg1 dramatically promoted angiogenesis and alleviated oxidative stress in the DFU mouse model and HG-induced HUVECs, thus accelerating wound healing. Importantly, miR-155-5p was proved to be upregulated in DFU wound tissues and HG-induced HUVECs, and overexpression of miR-155-5p remarkably impaired angiogenesis and stimulated oxidative stress in Rg1-administrated DFU mice and HG-induced HUVECs. Moreover, E2F2, a transcriptional activator of CDCA7L, was a direct downstream target of miR-155-5p. Rescue experiments showed that the reverse roles of miR-155-5p upregulation on Rg1-mediated oxidative stress repression and angiogenesis were obviously diminished by E2F2 downregulation.
CONCLUSION: Overall, our data revealed for the first time that Rg1 promoted wound healing in DFU via regulating miR-155-5p/E2F2/CDCA7L axis, which demonstrated a novel underlying mechanism of Rg1 in the treatment of DFU and provided some novel target for DFU therapy.
METHODS: A DFU mouse model was established, and wound healing was assessed using macroscopic observation and HE staining. The oxidative stress level was evaluated by ELISA and immunohistochemistry assays. In vitro, ELISA, RT-qPCR, CCK-8, transwell migration, and tube formation assays were used to evaluate oxidative stress, wound closure, and angiogenesis in high glucose (HG)-induced HUVECs, respectively. Dual luciferase-reporter assay determined the interaction between miR-155-5p and E2F2.
RESULTS: Here, we observed that Rg1 dramatically promoted angiogenesis and alleviated oxidative stress in the DFU mouse model and HG-induced HUVECs, thus accelerating wound healing. Importantly, miR-155-5p was proved to be upregulated in DFU wound tissues and HG-induced HUVECs, and overexpression of miR-155-5p remarkably impaired angiogenesis and stimulated oxidative stress in Rg1-administrated DFU mice and HG-induced HUVECs. Moreover, E2F2, a transcriptional activator of CDCA7L, was a direct downstream target of miR-155-5p. Rescue experiments showed that the reverse roles of miR-155-5p upregulation on Rg1-mediated oxidative stress repression and angiogenesis were obviously diminished by E2F2 downregulation.
CONCLUSION: Overall, our data revealed for the first time that Rg1 promoted wound healing in DFU via regulating miR-155-5p/E2F2/CDCA7L axis, which demonstrated a novel underlying mechanism of Rg1 in the treatment of DFU and provided some novel target for DFU therapy.