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Anti-inflammatory action of geniposide promotes wound healing in diabetic rats

CONTEXT: As a major active iridoid glycoside from Gardenia jasminoides J. Ellis (Rubiaceae), geniposide possesses various pharmacological activities, including anti-platelet aggregation and anti-inflammatory action. OBJECTIVES: This study explores the effect of geniposide in diabetic wound model by...

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Autores principales: Chen, Xiao-yan, Jiang, Wen-wen, Liu, Yan-ling, Ma, Zhao-xia, Dai, Jian-qiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8823683/
https://www.ncbi.nlm.nih.gov/pubmed/35130118
http://dx.doi.org/10.1080/13880209.2022.2030760
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author Chen, Xiao-yan
Jiang, Wen-wen
Liu, Yan-ling
Ma, Zhao-xia
Dai, Jian-qiang
author_facet Chen, Xiao-yan
Jiang, Wen-wen
Liu, Yan-ling
Ma, Zhao-xia
Dai, Jian-qiang
author_sort Chen, Xiao-yan
collection PubMed
description CONTEXT: As a major active iridoid glycoside from Gardenia jasminoides J. Ellis (Rubiaceae), geniposide possesses various pharmacological activities, including anti-platelet aggregation and anti-inflammatory action. OBJECTIVES: This study explores the effect of geniposide in diabetic wound model by anti-inflammatory action. MATERIALS AND METHODS: Diabetic rodent model in Wistar rats was induced by streptozotocin combined with high-fat feed. The selected rats were divided into control group, the diabetic model group and geniposide subgroups (200, 400 and 500 mg/kg), and orally administrated once daily with saline or geniposide. Wound area and histochemical indicators were measured on day 7 after continuous administration, to assess lesion retraction, inflammatory cells and fibroblasts. RESULTS: Geniposide notably enhanced lesion retraction by 1.06–1.84 times on day 7 after surgical onset in diabetic rats (p < 0.05). In the pathological experiment by HE staining, geniposide significantly reduced inflammatory cell infiltration and proliferation of fibroblasts in the central lesion regions. In diabetic rats treated with geniposide, the levels of pro-inflammatory factors (tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β)) and IL-6 were significantly reduced (p < 0.05), followed with the increment of IL-10 in a dose-dependent manner. The IC(50) of geniposide on TNF-α, IL-1β and IL-6 could be calculated as 1.36, 1.02 and 1.23 g/kg, respectively. It assumed that geniposide-induced IL-10 expression contributed to inhibiting the expression of pro-inflammatory factors. DISCUSSION AND CONCLUSIONS: Geniposide promoted diabetic wound healing by anti-inflammation and adjusting blood glucose. Further topical studies are required to evaluate effects on antibacterial activity and skin regeneration.
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spelling pubmed-88236832022-02-09 Anti-inflammatory action of geniposide promotes wound healing in diabetic rats Chen, Xiao-yan Jiang, Wen-wen Liu, Yan-ling Ma, Zhao-xia Dai, Jian-qiang Pharm Biol Research Article CONTEXT: As a major active iridoid glycoside from Gardenia jasminoides J. Ellis (Rubiaceae), geniposide possesses various pharmacological activities, including anti-platelet aggregation and anti-inflammatory action. OBJECTIVES: This study explores the effect of geniposide in diabetic wound model by anti-inflammatory action. MATERIALS AND METHODS: Diabetic rodent model in Wistar rats was induced by streptozotocin combined with high-fat feed. The selected rats were divided into control group, the diabetic model group and geniposide subgroups (200, 400 and 500 mg/kg), and orally administrated once daily with saline or geniposide. Wound area and histochemical indicators were measured on day 7 after continuous administration, to assess lesion retraction, inflammatory cells and fibroblasts. RESULTS: Geniposide notably enhanced lesion retraction by 1.06–1.84 times on day 7 after surgical onset in diabetic rats (p < 0.05). In the pathological experiment by HE staining, geniposide significantly reduced inflammatory cell infiltration and proliferation of fibroblasts in the central lesion regions. In diabetic rats treated with geniposide, the levels of pro-inflammatory factors (tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β)) and IL-6 were significantly reduced (p < 0.05), followed with the increment of IL-10 in a dose-dependent manner. The IC(50) of geniposide on TNF-α, IL-1β and IL-6 could be calculated as 1.36, 1.02 and 1.23 g/kg, respectively. It assumed that geniposide-induced IL-10 expression contributed to inhibiting the expression of pro-inflammatory factors. DISCUSSION AND CONCLUSIONS: Geniposide promoted diabetic wound healing by anti-inflammation and adjusting blood glucose. Further topical studies are required to evaluate effects on antibacterial activity and skin regeneration. Taylor & Francis 2022-02-07 /pmc/articles/PMC8823683/ /pubmed/35130118 http://dx.doi.org/10.1080/13880209.2022.2030760 Text en © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Chen, Xiao-yan
Jiang, Wen-wen
Liu, Yan-ling
Ma, Zhao-xia
Dai, Jian-qiang
Anti-inflammatory action of geniposide promotes wound healing in diabetic rats
title Anti-inflammatory action of geniposide promotes wound healing in diabetic rats
title_full Anti-inflammatory action of geniposide promotes wound healing in diabetic rats
title_fullStr Anti-inflammatory action of geniposide promotes wound healing in diabetic rats
title_full_unstemmed Anti-inflammatory action of geniposide promotes wound healing in diabetic rats
title_short Anti-inflammatory action of geniposide promotes wound healing in diabetic rats
title_sort anti-inflammatory action of geniposide promotes wound healing in diabetic rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8823683/
https://www.ncbi.nlm.nih.gov/pubmed/35130118
http://dx.doi.org/10.1080/13880209.2022.2030760
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