Zinc-sparing strategy for diabetic wound healing via GPR39 activation

Delayed wound healing in diabetes is exacerbated by chronic inflammation and impaired keratinocyte migration. While zinc promotes healing, excessive accumulation can be cytotoxic. This study investigates the synergistic effects of zinc and GPR39 agonist TC-G-1008 in diabetic wound repair. In vitro,...

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Published inInternational journal of oral biology Vol. 50; no. 2; pp. 53 - 63
Main Authors Lee, Jinu, Baek, Jeong-Hwa, Woo, Kyung Mi
Format Journal Article
LanguageEnglish
Published 대한구강생물학회 30.06.2025
Subjects
치의학
Online AccessGet full text
ISSN1226-7155
2287-6618
DOI10.11620/IJOB.2025.50.2.53

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Abstract Delayed wound healing in diabetes is exacerbated by chronic inflammation and impaired keratinocyte migration. While zinc promotes healing, excessive accumulation can be cytotoxic. This study investigates the synergistic effects of zinc and GPR39 agonist TC-G-1008 in diabetic wound repair. In vitro, co-treatment reduced LPS-induced pro-inflammatory cytokine expression and enhanced keratinocyte migration via ERK activation. In vivo, a hydrogel containing zinc oxide nanoparticles and TC-G-1008 accelerated wound closure in diabetic mice and downregulated il-1β expression. TC-G-1008 alone improved keratinocyte migration under diabetic conditions, indicating its pivotal role in modulating inflammation. These findings suggest a zinc-sparing therapeutic strategy using GPR39 agonism to restore wound healing in diabetic environments. KCI Citation Count: 0
AbstractList Delayed wound healing in diabetes is exacerbated by chronic inflammation and impaired keratinocyte migration. While zinc promotes healing, excessive accumulation can be cytotoxic. This study investigates the synergistic effects of zinc and GPR39 agonist TC-G-1008 in diabetic wound repair. In vitro, co-treatment reduced LPS-induced pro-inflammatory cytokine expression and enhanced keratinocyte migration via ERK activation. In vivo, a hydrogel containing zinc oxide nanoparticles and TC-G-1008 accelerated wound closure in diabetic mice and downregulated il-1β expression. TC-G-1008 alone improved keratinocyte migration under diabetic conditions, indicating its pivotal role in modulating inflammation. These findings suggest a zinc-sparing therapeutic strategy using GPR39 agonism to restore wound healing in diabetic environments. KCI Citation Count: 0
Author Woo, Kyung Mi
Baek, Jeong-Hwa
Lee, Jinu
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Title Zinc-sparing strategy for diabetic wound healing via GPR39 activation
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