title: Gallic Acid Promotes Wound Healing in Normal and Hyperglucidic Conditions.
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.
authors.affiliation: Department of Pharmacology, Wonju College of Medicine, Yonsei University, Wonju 26426, Korea. ydj1991@yonsei.ac.kr.|Department of Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju 26426, Korea. ydj1991@yonsei.ac.kr.
authors.forename: Dong Joo
authors.initials: DJ
authors.lastname: Yang
authors.affiliation: Anti-Aging Research Institute of BIO-FD &amp; C Co. Ltd., Incheon 21990, Korea. biofdnc@gmail.com.
authors.forename: Sang Hyun
authors.initials: SH
authors.lastname: Moh
authors.affiliation: Department of Pharmacology, Wonju College of Medicine, Yonsei University, Wonju 26426, Korea. donghweeson@gmail.com.|Department of Wellness &amp; Healthy Aging, Wonju College of Medicine, Yonsei University, Wonju 26426, Korea. donghweeson@gmail.com.
authors.forename: Dong Hwee
authors.initials: DH
authors.lastname: Son
authors.affiliation: Department of Pharmacology, Wonju College of Medicine, Yonsei University, Wonju 26426, Korea. bloodship90@naver.com.
authors.forename: Seunghoon
authors.initials: S
authors.lastname: You
authors.affiliation: Department of Pharmacology, Wonju College of Medicine, Yonsei University, Wonju 26426, Korea. annmendi@gmail.com.|Department of Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju 26426, Korea. annmendi@gmail.com.
authors.forename: Ann W
authors.initials: AW
authors.lastname: Kinyua
authors.affiliation: Department of Pharmacology, Wonju College of Medicine, Yonsei University, Wonju 26426, Korea. changmko@yonsei.ac.kr.
authors.forename: Chang Mann
authors.initials: CM
authors.lastname: Ko
authors.affiliation: Anti-Aging Research Institute of BIO-FD &amp; C Co. Ltd., Incheon 21990, Korea. mysong@biofdnc.com.
authors.forename: Miyoung
authors.initials: M
authors.lastname: Song
authors.affiliation: Jeongseon Agricultural Extension Center, Jeongseon 26103, Korea. 1257@korea.kr.
authors.forename: Jinhee
authors.initials: J
authors.lastname: Yeo
authors.affiliation: Anti-Aging Research Institute of BIO-FD &amp; C Co. Ltd., Incheon 21990, Korea. imyunhee@gmail.com.
authors.forename: Yun-Hee
authors.initials: YH
authors.lastname: Choi
authors.affiliation: Department of Pharmacology, Wonju College of Medicine, Yonsei University, Wonju 26426, Korea. kiwoo@yonsei.ac.kr.|Department of Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju 26426, Korea. kiwoo@yonsei.ac.kr.
authors.forename: Ki Woo
authors.initials: KW
authors.lastname: Kim
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology; D001713:Biphenyl Compounds / Q000037:antagonists & inhibitors; D002374:Catalase / Q000235:genetics / Q000378:metabolism; D002460:Cell Line; D002465:Cell Movement / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D005347:Fibroblasts / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D051417:Focal Adhesion Kinase 1 / Q000235:genetics / Q000378:metabolism; D005707:Gallic Acid / Q000494:pharmacology*; D005786:Gene Expression Regulation; D005947:Glucose / Q000037:antagonists & inhibitors* / Q000378:metabolism / Q000633:toxicity; D005979:Glutathione Peroxidase / Q000235:genetics / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000037:antagonists & inhibitors / Q000494:pharmacology; D015603:Keratinocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D048670:MAP Kinase Kinase 4 / Q000235:genetics / Q000378:metabolism; D051379:Mice; D019950:Mitogen-Activated Protein Kinase 1 / Q000235:genetics / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000235:genetics / Q000378:metabolism; D008954:Models, Biological; D010851:Picrates / Q000037:antagonists & inhibitors; D015398:Signal Transduction; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D014945:Wound Healing / Q000187:drug effects*
chemical_list: D000975:Antioxidants; D001713:Biphenyl Compounds; D010851:Picrates; D005707:Gallic Acid; D006861:Hydrogen Peroxide; C004931:1,1-diphenyl-2-picrylhydrazyl; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D051417:Focal Adhesion Kinase 1; C496050:PTK2 protein, human; C535150:MAPK1 protein, human; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D048670:MAP Kinase Kinase 4; D005947:Glucose; D001205:Ascorbic Acid
keywords: cell migration; gallic acid; hyperglucidic condition; wound healing