Gallic Acid Promotes Wound Healing in Normal and Hyperglucidic Conditions

Dong Joo Yang, Sang Hyun Moh, Dong Hwee Son, Seunghoon You, Ann W. Kinyua, Chang Mann Ko, Miyoung Song, Jinhee Yeo, Yun Hee Choi, Ki Woo Kim

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Skin is the outermost layer of the human body that is constantly exposed to environmental stressors, such as UV radiation and toxic chemicals, and is susceptible to mechanical wounding and injury. The ability of the skin to repair injuries is paramount for survival and it is disrupted in a spectrum of disorders leading to skin pathologies. Diabetic patients often suffer from chronic, impaired wound healing, which facilitate bacterial infections and necessitate amputation. Here, we studied the effects of gallic acid (GA, 3,4,5-trihydroxybenzoic acid; a plant-derived polyphenolic compound) on would healing in normal and hyperglucidic conditions, to mimic diabetes, in human keratinocytes and fibroblasts. Our study reveals that GA is a potential antioxidant that directly upregulates the expression of antioxidant genes. In addition, GA accelerated cell migration of keratinocytes and fibroblasts in both normal and hyperglucidic conditions. Further, GA treatment activated factors known to be hallmarks of wound healing, such as focal adhesion kinases (FAK), c-Jun N-terminal kinases (JNK), and extracellular signal-regulated kinases (Erk), underpinning the beneficial role of GA in wound repair. Therefore, our results demonstrate that GA might be a viable wound healing agent and a potential intervention to treat wounds resulting from metabolic complications.

Original languageEnglish
Article number899
JournalMolecules
Volume21
Issue number7
DOIs
Publication statusPublished - 2016 Jul

Fingerprint

wound healing
Gallic Acid
Wound Healing
Skin
fibroblasts
antioxidants
Fibroblasts
acids
Wounds and Injuries
Repair
Polyphenolic compounds
Antioxidants
Keratinocytes
Focal Adhesion Protein-Tyrosine Kinases
JNK Mitogen-Activated Protein Kinases
Poisons
Extracellular Signal-Regulated MAP Kinases
healing
pathology
human body

All Science Journal Classification (ASJC) codes

  • Analytical Chemistry
  • Chemistry (miscellaneous)
  • Molecular Medicine
  • Pharmaceutical Science
  • Drug Discovery
  • Physical and Theoretical Chemistry
  • Organic Chemistry

Cite this

Yang, D. J., Moh, S. H., Son, D. H., You, S., Kinyua, A. W., Ko, C. M., ... Kim, K. W. (2016). Gallic Acid Promotes Wound Healing in Normal and Hyperglucidic Conditions. Molecules, 21(7), [899]. https://doi.org/10.3390/molecules21070899
Yang, Dong Joo ; Moh, Sang Hyun ; Son, Dong Hwee ; You, Seunghoon ; Kinyua, Ann W. ; Ko, Chang Mann ; Song, Miyoung ; Yeo, Jinhee ; Choi, Yun Hee ; Kim, Ki Woo. / Gallic Acid Promotes Wound Healing in Normal and Hyperglucidic Conditions. In: Molecules. 2016 ; Vol. 21, No. 7.
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abstract = "Skin is the outermost layer of the human body that is constantly exposed to environmental stressors, such as UV radiation and toxic chemicals, and is susceptible to mechanical wounding and injury. The ability of the skin to repair injuries is paramount for survival and it is disrupted in a spectrum of disorders leading to skin pathologies. Diabetic patients often suffer from chronic, impaired wound healing, which facilitate bacterial infections and necessitate amputation. Here, we studied the effects of gallic acid (GA, 3,4,5-trihydroxybenzoic acid; a plant-derived polyphenolic compound) on would healing in normal and hyperglucidic conditions, to mimic diabetes, in human keratinocytes and fibroblasts. Our study reveals that GA is a potential antioxidant that directly upregulates the expression of antioxidant genes. In addition, GA accelerated cell migration of keratinocytes and fibroblasts in both normal and hyperglucidic conditions. Further, GA treatment activated factors known to be hallmarks of wound healing, such as focal adhesion kinases (FAK), c-Jun N-terminal kinases (JNK), and extracellular signal-regulated kinases (Erk), underpinning the beneficial role of GA in wound repair. Therefore, our results demonstrate that GA might be a viable wound healing agent and a potential intervention to treat wounds resulting from metabolic complications.",
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Yang, DJ, Moh, SH, Son, DH, You, S, Kinyua, AW, Ko, CM, Song, M, Yeo, J, Choi, YH & Kim, KW 2016, 'Gallic Acid Promotes Wound Healing in Normal and Hyperglucidic Conditions', Molecules, vol. 21, no. 7, 899. https://doi.org/10.3390/molecules21070899

Gallic Acid Promotes Wound Healing in Normal and Hyperglucidic Conditions. / Yang, Dong Joo; Moh, Sang Hyun; Son, Dong Hwee; You, Seunghoon; Kinyua, Ann W.; Ko, Chang Mann; Song, Miyoung; Yeo, Jinhee; Choi, Yun Hee; Kim, Ki Woo.

In: Molecules, Vol. 21, No. 7, 899, 07.2016.

Research output: Contribution to journalArticle

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AU - You, Seunghoon

AU - Kinyua, Ann W.

AU - Ko, Chang Mann

AU - Song, Miyoung

AU - Yeo, Jinhee

AU - Choi, Yun Hee

AU - Kim, Ki Woo

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N2 - Skin is the outermost layer of the human body that is constantly exposed to environmental stressors, such as UV radiation and toxic chemicals, and is susceptible to mechanical wounding and injury. The ability of the skin to repair injuries is paramount for survival and it is disrupted in a spectrum of disorders leading to skin pathologies. Diabetic patients often suffer from chronic, impaired wound healing, which facilitate bacterial infections and necessitate amputation. Here, we studied the effects of gallic acid (GA, 3,4,5-trihydroxybenzoic acid; a plant-derived polyphenolic compound) on would healing in normal and hyperglucidic conditions, to mimic diabetes, in human keratinocytes and fibroblasts. Our study reveals that GA is a potential antioxidant that directly upregulates the expression of antioxidant genes. In addition, GA accelerated cell migration of keratinocytes and fibroblasts in both normal and hyperglucidic conditions. Further, GA treatment activated factors known to be hallmarks of wound healing, such as focal adhesion kinases (FAK), c-Jun N-terminal kinases (JNK), and extracellular signal-regulated kinases (Erk), underpinning the beneficial role of GA in wound repair. Therefore, our results demonstrate that GA might be a viable wound healing agent and a potential intervention to treat wounds resulting from metabolic complications.

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