Journal Article

Gallic Acid Promotes Wound Healing in Normal and Hyperglucidic Conditions

Ko, Chang, Son, Dong, Yeo, Jinhee, Kim, Ki, You, Seunghoon, Song, Miyoung, Choi, Yun-Hee, Kinyua, Ann, Yang, Dong, Moh, Sang

2016

Overview

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.

• Publisher: MDPI AG,MDPI
• Subject: Acids / Animals / Antioxidants / Antioxidants - pharmacology / Ascorbic Acid - pharmacology / Bacterial infections / Biphenyl Compounds - antagonists & inhibitors / Catalase - genetics / Catalase - metabolism / Cell adhesion & migration / Cell Line / cell migration / Cell Movement - drug effects / Cell Survival - drug effects / Cytotoxicity / Diabetes / Fibroblasts - cytology / Fibroblasts - drug effects / Fibroblasts - metabolism / Focal Adhesion Kinase 1 - genetics / Focal Adhesion Kinase 1 - metabolism / gallic acid / Gallic Acid - pharmacology / Gene Expression Regulation / Glucose - antagonists & inhibitors / Glucose - metabolism / Glucose - toxicity / Glutathione Peroxidase - genetics / Glutathione Peroxidase - metabolism / Humans / Hydrogen Peroxide - antagonists & inhibitors / Hydrogen Peroxide - pharmacology / hyperglucidic condition / Hyperglycemia / Infections / Injuries / Keratinocytes - cytology / Keratinocytes - drug effects / Keratinocytes - metabolism / MAP Kinase Kinase 4 - genetics / MAP Kinase Kinase 4 - metabolism / Metabolism / Mice / Mitogen-Activated Protein Kinase 1 - genetics / Mitogen-Activated Protein Kinase 1 - metabolism / Mitogen-Activated Protein Kinase 3 - genetics / Mitogen-Activated Protein Kinase 3 - metabolism / Models, Biological / Natural products / Oxidative stress / Picrates - antagonists & inhibitors / Polyphenols / Signal Transduction / Skin / Superoxide Dismutase - genetics / Superoxide Dismutase - metabolism / Trauma / Wound healing / Wound Healing - drug effects