通过Nrf2-介导的铁亡路促进热烧伤愈合的Tectorigenin机制:综合药理和实验研究
Aneela Bashir1, Wang Mei2, Lingnan Zhang3
1Key Laboratory of Biorheological Science and Technology of Ministry of Education, Bioengineering College, Chongqing University, Chongqing, 400044, China.
International journal of biological macromolecules
|December 26, 2025
概括
原蛋白 (TG) 通过激活Nrf2通路,加速烧伤愈合,减少氧化应激和炎症. 这种天然化合物通过抗氧化和抗ferroptotic机制促进皮肤修复.
科学领域:
- 皮肤病学 皮肤病学
- 药理学 药理学是指药理学的学科.
- 生物化学 生物化学
背景情况:
- 热烧伤会造成严重的皮肤损伤,由于氧化应激,炎症和铁灭症而延迟愈合.
- 来自Belamcanda chinensis的异黄Tectorigenin (TG) 已知具有抗氧化和抗炎性质,但其在烧伤修复中的作用尚不清楚.
研究的目的:
- 调查Tectorigenin (TG) 在促进烧伤愈合方面的治疗潜力和分子机制.
主要方法:
- 网络药理学分析以预测TG目标和途径.
- 使用小鼠部分厚度烧伤模型的体内研究.
- 在H2O2刺激的HaCaT细胞的体外实验.
主要成果:
- 在体内,TG加速了伤口收缩,原重塑和新血管化.
- TG激活了Nrf2-HO-1/SLC7A11/GPX4轴,减少了炎症性细胞因子 (TNF-α,IL-6),并增加了VEGF.
- 在体外,TG通过抑制依赖Nrf2激活的氧化应激和脂质过氧化来保护HaCaT细胞.
结论:
- 原蛋白 (TG) 通过激活Nrf2介导的抗氧化和抗ferroptotic防御,有效促进烧伤愈合.
- TG调节炎症和血管生成,作为氧化应激相关皮肤损伤的天然治疗方法有希望.
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