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作 者:Wu-Han Wei Yuan-Ling Bai Dong Zhu Jing-Yu Zhang Qi-Chuan Yin Qiang Li Cai-Qi Shen Pei-Sheng Jin
机构地区:[1]The First Clinical Medical College,Xuzhou Medical University,Xuzhou 221004,Jiangsu Province,China [2]Plastic Surgery Hospital,Chinese Academy of Medical Sciences,Peking Union Medical College,Beijing 100144,China [3]Department of Plastic Surgery,Affiliated Hospital of Xuzhou Medical University,Xuzhou 221006,Jiangsu Province,China
出 处:《World Journal of Diabetes》2025年第4期252-269,共18页世界糖尿病杂志(英文)
基 金:Supported by General Project of Xuzhou Science and Technology Bureau,No.KC22070.
摘 要:BACKGROUND Diabetic foot ulcers(DFU)are estimated to affect about 18.6 million people worldwide annually.The pathogenesis of DFU is complex,and the available drugs are not effective.Dl-3-n-butylphthalide(NBP)is a synthetic mixture of racemates used in China for the treatment of ischemic stroke.It was initially isolated from the seeds of Apium graveolens Linn,with studies showing its potential role in treating diabetes and its complications.AIM To predict and validate the mechanism by which NBP treats DFU.METHODS Network pharmacological analysis was performed to identify pharmacological targets and signaling pathways mediating the treatment effect of NBP on DFU.In vivo and in vitro experiments were conducted to validate the therapeutic effects and mechanisms of NBP on DFU.RESULTS Network pharmacology analysis identified 26 pharmacological targets of NBP and predicted that NBP could treat DFU partially by modulating apoptosis and vascular signaling pathways.Results from animal experiments showed that NBP significantly improved DFU by increasing neovascularization and fibroblast proliferation.In vitro tests demonstrated that NBP treatment promoted the migration and proliferation of human umbilical vein endothelial cells and human dermal fibroblasts,while inhibiting the apoptosis of human umbilical vein endothelial cells,human dermal fibroblasts,and human keratinocytes cells.CONCLUSION This study found that NBP could treat DFU by decreasing the rate of apoptosis and increasing angiogenesis via the advanced glycation end products-receptor of advanced glycation end products signaling pathway and binding to the heme oxygenase 1,caspase 3,B cell leukemia/lymphoma 2,brain derived neurotrophic factor,and nuclear factor erythroid 2 L2 genes.
关 键 词:Dl-3-n-butylphthalide Diabetic foot ulcer Network pharmacology ANGIOGENESIS APOPTOSIS
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