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Geniposide promotes wound healing of skin ulcers in diabetic rats through PI3K/Akt pathway

Continuously hyperglycation-induced lesion and poor blood flow contributed to the wound incurable and susceptible to infection. About fifteen percent of people with diabetes would develop ulcers during their lifetime, especially on the feet, which could lead to severe tissue destruction and eventual...

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Autores principales: Fang, Chun-juan, Rong, Xiao-juan, Jiang, Wen-wen, Chen, Xiao-yan, Liu, Yan-ling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10613912/
https://www.ncbi.nlm.nih.gov/pubmed/37908704
http://dx.doi.org/10.1016/j.heliyon.2023.e21331
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author Fang, Chun-juan
Rong, Xiao-juan
Jiang, Wen-wen
Chen, Xiao-yan
Liu, Yan-ling
author_facet Fang, Chun-juan
Rong, Xiao-juan
Jiang, Wen-wen
Chen, Xiao-yan
Liu, Yan-ling
author_sort Fang, Chun-juan
collection PubMed
description Continuously hyperglycation-induced lesion and poor blood flow contributed to the wound incurable and susceptible to infection. About fifteen percent of people with diabetes would develop ulcers during their lifetime, especially on the feet, which could lead to severe tissue destruction and eventual amputation. Various strategies were limited to accelerate wound healing in diabetic patients for high cost and unsatisfied effects. Geniposide is well-known for its anti-inflammation and anti-apoptosis in several pathological tissues. This study is to explore the protective effect of geniposide on wound healing rate, inflammatory response, nutritional function and cellular apoptosis in diabetic rats. Diabetic rats was induced by streptozotocin and defined as plasma glucose >300 mg/dl. Western blot and immunostaining technologies were performed to mark and quantify the target proteins. The oral administration of geniposide (200 mg/kg and 500 mg/kg) could significantly promote wound healing by the increment of lesion retraction in diabetic rats compared to model group. In the apoptotic study of skin wound in diabetic rats, the TUNEL-positive cells were greatly decreased in geniposide subgroups (P < 0.05). The levels of TNF-α, IL-1β and IL-6 were significantly inhibited by geniposide with the IC(50) value of 470 mg/kg, 464 mg/kg and 370 mg/kg body weight respectively, which might be related to the enhancement of the phosphorylation of PI3K and Akt proteins. Geniposide enhanced the repairment of skin wound in diabetic rats by inhibiting inflammatory response and apoptosis.
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spelling pubmed-106139122023-10-31 Geniposide promotes wound healing of skin ulcers in diabetic rats through PI3K/Akt pathway Fang, Chun-juan Rong, Xiao-juan Jiang, Wen-wen Chen, Xiao-yan Liu, Yan-ling Heliyon Research Article Continuously hyperglycation-induced lesion and poor blood flow contributed to the wound incurable and susceptible to infection. About fifteen percent of people with diabetes would develop ulcers during their lifetime, especially on the feet, which could lead to severe tissue destruction and eventual amputation. Various strategies were limited to accelerate wound healing in diabetic patients for high cost and unsatisfied effects. Geniposide is well-known for its anti-inflammation and anti-apoptosis in several pathological tissues. This study is to explore the protective effect of geniposide on wound healing rate, inflammatory response, nutritional function and cellular apoptosis in diabetic rats. Diabetic rats was induced by streptozotocin and defined as plasma glucose >300 mg/dl. Western blot and immunostaining technologies were performed to mark and quantify the target proteins. The oral administration of geniposide (200 mg/kg and 500 mg/kg) could significantly promote wound healing by the increment of lesion retraction in diabetic rats compared to model group. In the apoptotic study of skin wound in diabetic rats, the TUNEL-positive cells were greatly decreased in geniposide subgroups (P < 0.05). The levels of TNF-α, IL-1β and IL-6 were significantly inhibited by geniposide with the IC(50) value of 470 mg/kg, 464 mg/kg and 370 mg/kg body weight respectively, which might be related to the enhancement of the phosphorylation of PI3K and Akt proteins. Geniposide enhanced the repairment of skin wound in diabetic rats by inhibiting inflammatory response and apoptosis. Elsevier 2023-10-23 /pmc/articles/PMC10613912/ /pubmed/37908704 http://dx.doi.org/10.1016/j.heliyon.2023.e21331 Text en © 2023 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Research Article
Fang, Chun-juan
Rong, Xiao-juan
Jiang, Wen-wen
Chen, Xiao-yan
Liu, Yan-ling
Geniposide promotes wound healing of skin ulcers in diabetic rats through PI3K/Akt pathway
title Geniposide promotes wound healing of skin ulcers in diabetic rats through PI3K/Akt pathway
title_full Geniposide promotes wound healing of skin ulcers in diabetic rats through PI3K/Akt pathway
title_fullStr Geniposide promotes wound healing of skin ulcers in diabetic rats through PI3K/Akt pathway
title_full_unstemmed Geniposide promotes wound healing of skin ulcers in diabetic rats through PI3K/Akt pathway
title_short Geniposide promotes wound healing of skin ulcers in diabetic rats through PI3K/Akt pathway
title_sort geniposide promotes wound healing of skin ulcers in diabetic rats through pi3k/akt pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10613912/
https://www.ncbi.nlm.nih.gov/pubmed/37908704
http://dx.doi.org/10.1016/j.heliyon.2023.e21331
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