级联Co8FeS8@Co1-xS纳米酶可以有效地触发亡-费洛亡组合瘤治疗
Liling Wang1, Tao Wang1, Yong Zhuo2
1College of Science, Sichuan Agricultural University, Xin Kang Road, Yucheng District, Ya'an 625014, PR China.
Journal of colloid and interface science
|February 21, 2024
概括
新型Co8FeS8@Co1-xS纳米酶利用双重活动来治疗瘤. 它们通过产生基基和耗尽谷氨来诱导亡和铁亡,向KRAS突变的癌细胞.
科学领域:
- 生物材料科学 生物材料科学
- 纳米技术纳米技术
- 癌症治疗 癌症治疗
背景情况:
- 金属有机框架 (MOF) 为纳米材料合成提供了多功能平台.
- 开发有效的纳米酶用于癌症治疗是研究的一个关键领域.
- 向亡和铁亡都是克服治疗耐药性的有希望的策略.
研究的目的:
- 为了合成和描述MOF衍生的Co8FeS8@Co1-xS纳米酶.
- 为了研究纳米酶的双重过氧化酶样和减少的谷氨氧化活性.
- 评估这些纳米酶对抗抗亡性瘤细胞的协同治疗潜力,特别是具有KRAS突变的瘤细胞.
主要方法:
- 从MOF中制备Co8FeS8@Co1-xS纳米酶.
- 测定过氧化酶 (POD) 类活性和降低的谷氨 (GSH) 氧化.
- 在体外评估基 (•OH) 生产和GSH耗尽.
- 通过BCL-2抑制和卡斯帕酶激活来评估亡诱导.
- 分析铁代谢基因表达 (例如Hmox-1) 和芬顿反应.
- 对铁灭症诱导机制的研究.
- 在KRAS突变癌症模型中评估生物相容性和抗瘤功效.
主要成果:
- 成功合成了MOF衍生的Co8FeS8@Co1-xS纳米酶,具有强大的界面相互作用.
- 纳米酶表现出显著的POD类活性和GSH氧化能力.
- 双重活动导致增强OH生产和GSH耗尽,诱导了亡和铁亡.
- 纳米酶抑制了抗亡蛋白Bcl-2并激活了亡酶,促进了亡.
- 铁代谢基因 (Hmox-1) 的调节放大了芬顿反应,增强了细胞死亡.
- 观察到有效的协同杀死具有KRAS突变的抗亡性瘤细胞.
- 这些纳米酶显示出良好的生物相容性.
结论:
- Co8FeS8@Co1-xS纳米酶为瘤治疗提供了一个自我级联的催化平台.
- 双重活性纳米酶有效诱导瘤细胞的亡和铁亡.
- 这种方法对针对具有挑战性的抗断性和KRAS突变瘤显得有前途.
- 开发的纳米酶平台为有效的癌症治疗提供了潜在的战略.
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