Zinc-sparing strategy for diabetic wound healing via GPR39 activation

• Published in: International journal of oral biology Vol. 50; no. 2; pp. 53 - 63
• Main Authors: Lee, Jinu, Baek, Jeong-Hwa, Woo, Kyung Mi
• Format: Journal Article
• Language: English
• Published: 대한구강생물학회 30.06.2025
• Subjects: 치의학
• ISSN: 1226-7155; 2287-6618
• DOI: 10.11620/IJOB.2025.50.2.53

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