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Astragalus Polysaccharides Promote Wound Healing in Diabetic Rats by Upregulating PETN and Inhibiting the mTOR Pathway

OBJECTIVE: Presently, astragalus polysaccharide (APS) is being investigated for its therapeutic potential in various diseases; however, its underlying mechanism has not yet been clarified. This study was aimed at observing the effects of APS on wound healing in diabetic rats and at exploring its und...

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Detalles Bibliográficos
Autor principal: Ma, Le
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9586772/
https://www.ncbi.nlm.nih.gov/pubmed/36277005
http://dx.doi.org/10.1155/2022/3459102
Descripción
Sumario:OBJECTIVE: Presently, astragalus polysaccharide (APS) is being investigated for its therapeutic potential in various diseases; however, its underlying mechanism has not yet been clarified. This study was aimed at observing the effects of APS on wound healing in diabetic rats and at exploring its underlying mechanism. METHODS: Streptozotocin was injected into the tail vein of SD rats to induce diabetic animal models, in which an incision on the back was made. Rats were treated with different dosages of APS to observe their wound healing. Additionally, RT-qPCR and Western blot assay were conducted to observe the expression levels of PTEN and mTOR pathway-associated factors. RESULTS: Diabetic rats had a prolonged wound healing process, fewer blood vessels, and increased inflammatory response, in which decreased PTEN and elevated mTOR phosphorylation were also identified. APS effectively improved wound healing in a dose-dependent manner by inhibiting the release of inflammatory mediators and attenuating endothelial injuries. Suppression of PTEN could effectively increase the phosphorylation of mTOR and diminish the therapeutic functions of APS on wound healing in diabetic rats. CONCLUSION: This study highlighted that APS could promote wound healing in diabetic rats by upregulating PTEN and suppressing the mTOR pathway activation.