Circle RNA STT3B对糖尿病创面愈合的作用及机制研究
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1.徐州医科大学;2.徐州医科大学附属医院

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国家自然科学基金面上项目(82172224);徐州市卫健委医学科技创新面上项目(XWKYHT20230063)


Research on the Role and Mechanism of Circle RNA STT3B in Diabetic Wound Healing
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1.Xuzhou Medical University;2.XUZHOU medical university;3.Affiliated Hospital of Xuzhou Medical University

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    摘要:

    目的 探讨人源毛囊真皮干细胞外泌体(HFDSC-Exos)中环状RNA STT3B(circle RNA STT3B)对人角质形成细胞(HaCat)氧化应激损伤的保护及糖尿病创面愈合的作用,阐明其潜在分子机制。方法 通过检测氧化应激相关因子明确HFDSC-Exos对HaCat抗氧化作用;RNA-Pull down、ELISA、qPCR等实验探究circRNA STT3B与BACH1的相互作用及对HO-1的调控;建立糖尿病小鼠创面模型,观察circRNA STT3B对创面愈合的影响。结果 健康者HFDSC-Exos显著减少HaCat氧化应激因子水平(P<0.05)。 circRNA STT3B可与BACH1蛋白结合,导致BACH1入核减少,HO-1表达增加(P<0.05)。糖尿病小鼠创面实验显示,circRNA STT3B过表达组创面愈合速度更快,上皮细胞增生明显,胶原蛋白沉积丰富(P<0.05)。结论 HFDSC-Exos circRNA STT3B通过与HaCat细胞质中BACH1结合,导致BACH1入核减少,解除了HO-1等抗氧化应激因子的抑制,HO-1表达增加,减轻HaCat氧化应激损伤,促进糖尿病小鼠创面愈合。

    Abstract:

    ObjectiveSTo investigate the protective effect of circular RNA STT3B (circRNA STT3B) from human hair follicle dermal stem cell-derived exosomes (HFDSC-Exos) against oxidative stress damage in human keratinocytes (HaCat) and its role in diabetic wound healing, and to elucidate the underlying molecular mechanisms. MethodsSThe antioxidant effect of HFDSC-Exos on HaCat cells was determined by measuring oxidative stress-related factors. RNA pull-down, ELISA, and qPCR were used to explore the interaction between circRNA STT3B and BACH1 and its regulation of HO-1. A diabetic mouse wound model was established to observe the impact of circRNA STT3B on wound healing. ResultsSHFDSC-Exos from healthy donors significantly reduced oxidative stress factor levels in HaCat cells (P<0.05). CircRNA STT3B bound to BACH1 protein, reducing BACH1 nuclear translocation and increasing HO-1 expression (P<0.05). In diabetic mice, circRNA STT3B overexpression accelerated wound healing, enhanced epithelial cell proliferation, and increased collagen deposition (P<0.05).ConclusionSHFDSC-Exos circRNA STT3B binds to BACH1 in the cytoplasm of HaCat cells, inhibiting BACH1 nuclear entry and thereby relieving its suppression of antioxidant factors (e.g., HO-1). This upregulates HO-1 expression, mitigates oxidative stress damage in HaCat cells, and promotes diabetic wound healing.

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  • 收稿日期:2026-01-08
  • 最后修改日期:2026-03-22
  • 录用日期:2026-09-03
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