生物启发的超分子凝抑制铁灭,以加速糖尿病伤口愈合
Haiting Zou1, Jingyi Chen2, Yumeng Huang1
1Department of Burn and Plastic Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210009, China.
Journal of advanced research
|January 14, 2026
概括
拜卡林 (Bai) 通过调节Keap1/NRF2/HIF-1α轴,抑制内皮细胞中的铁亡,加速糖尿病伤口愈合. 一种新的水凝配方增强了Bai的输送和治疗疗效,用于糖尿病伤口修复.
科学领域:
- 生物材料科学 生物材料科学
- 细胞生物学 细胞生物学
- 伤口治愈研究研究 伤口治愈研究
背景情况:
- 铁性严重损害糖尿病伤口愈合,呈现一个关键的治疗目标.
- 拜卡莱因 (Bai),一种天然的黄类化合物,在调节铁亡方面表现出潜力,但其机制尚未完全理解.
研究的目的:
- 阐明Baicalein在内皮细胞中抑制铁亡的分子机制.
- 开发和验证含有Baicalein的水凝,以改善糖尿病伤口愈合.
主要方法:
- 研究了Baicalein在高葡萄糖诱导的人类带静脉内皮细胞 (HUVECs) 中抑制铁的机制.
- 开发了一种超分子纳米纤维水凝 (Bai@GA/Gel/Zn2+) 用于持续的Baicalein输送.
- 在糖尿病老鼠伤口模型中评估了水凝的治疗疗效和机制.
主要成果:
- 拜卡莱因抑制了HUVEC中高葡萄糖诱导的铁,促进细胞生长,迁移和血管生成.
- 拜卡莱因的机制涉及调节Keap1/NRF2/HIF-1α信号轴.
- Bai@GA/Gel/Zn2+水凝表现出有利的特性,降低了铁亡,并加速了糖尿病伤口愈合.
结论:
- 拜卡莱因通过Keap1/NRF2/HIF-1α通路有效抑制铁.
- 一种含有Baicalein的新型水凝通过持续的药物输送和铁灭抑制,协同增强糖尿病伤口愈合.
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