Journal of ethnopharmacology · 2025
Decoding the pharmacodynamics of Fufang Tongye Shaoshang You: A promising ethnomedicine for diabetic ulcer healing.
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Lu Yuting, Duan Yan, Dai Yuping, Ni Xiaoting, Li Juan, Zeng Xinliang, Cai Pei, Li Shunxiang
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Fufang Tongye Shaoshang You (TYY) is an ethnomedicine derived from the traditional folk formula of the Tujia people in Hunan Province, which consists of Paulownia leaf and sesame oil, has shown promising potential in promoting diabetic ulcer (DU) healing. However, its pharmacological substance and mechanism of action require further elucidation.
AIMS OF THE STUDY: This study was designed to assess the healing effect of TYY on DU wounds in mice, and to explore systematically its potential mechanisms and pharmacodynamic material basis.
METHODS: The combination of high-fat, high-sugar diet and streptozotocin injection was used to induce C57BL/6 J mouse diabetic model, and the ulcer was surgically introduced. After TYY treatment, the skin lesions of diabetic mice were observed by H&E, Masson staining and transmission electron microscopy over a period of time. The wound tissues were collected. Transcriptomics were used to predict the potential mechanism of TYY, and then immunohistochemistry, immunofluorescence, ELISA, Western blotting, and qRT-PCR were used to detect the expression levels of key proteins and mRNA in related signaling pathways. The effect of TYY on tight junction proteins was evaluated by Western blotting. The chemical components of 10 batches of TYY were analyzed by multivariate analysis, and the iconic components of TYY were screened by molecular docking and dynamics simulation. HMEC-1 cells were induced by lipopolysaccharide and high glucose concentrations to simulate a DU microenvironment and construct an endothelial cell injury model. Scratch test and RT-qPCR were used to evaluate the effects of TYY active ingredients on the endothelial cell injury model, finally determining the pharmacodynamic material basis of TYY.
RESULTS: The study has demonstrated that TYY can not only effectively repair the skin barrier, but also regulate the IL-17-mediated NF-κB/AP-1 signaling pathway, inhibit the exacerbation of inflammation, and accelerate wound healing in DU mice. In addition, we further discovered the key active ingredients of TYY: maslinic acid, corosolic acid, oleanolic acid, ursolic acid and sesamin.
CONCLUSION: This study provides scientific evidence for TYY as a potential drug to repair DU, and also provides a theoretical basis for its further clinical application and drug development.
AIMS OF THE STUDY: This study was designed to assess the healing effect of TYY on DU wounds in mice, and to explore systematically its potential mechanisms and pharmacodynamic material basis.
METHODS: The combination of high-fat, high-sugar diet and streptozotocin injection was used to induce C57BL/6 J mouse diabetic model, and the ulcer was surgically introduced. After TYY treatment, the skin lesions of diabetic mice were observed by H&E, Masson staining and transmission electron microscopy over a period of time. The wound tissues were collected. Transcriptomics were used to predict the potential mechanism of TYY, and then immunohistochemistry, immunofluorescence, ELISA, Western blotting, and qRT-PCR were used to detect the expression levels of key proteins and mRNA in related signaling pathways. The effect of TYY on tight junction proteins was evaluated by Western blotting. The chemical components of 10 batches of TYY were analyzed by multivariate analysis, and the iconic components of TYY were screened by molecular docking and dynamics simulation. HMEC-1 cells were induced by lipopolysaccharide and high glucose concentrations to simulate a DU microenvironment and construct an endothelial cell injury model. Scratch test and RT-qPCR were used to evaluate the effects of TYY active ingredients on the endothelial cell injury model, finally determining the pharmacodynamic material basis of TYY.
RESULTS: The study has demonstrated that TYY can not only effectively repair the skin barrier, but also regulate the IL-17-mediated NF-κB/AP-1 signaling pathway, inhibit the exacerbation of inflammation, and accelerate wound healing in DU mice. In addition, we further discovered the key active ingredients of TYY: maslinic acid, corosolic acid, oleanolic acid, ursolic acid and sesamin.
CONCLUSION: This study provides scientific evidence for TYY as a potential drug to repair DU, and also provides a theoretical basis for its further clinical application and drug development.