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丁硫酸盐功能化纳米酶通过调节细胞间交叉电路来抑制炎症反循环,以增强动脉样硬化治疗

Chenglong Wang¹, Yufeng He², Jun Tang³

¹Department of Pharmaceutical Sciences, School of Pharmacy, Southwest Medical University, Luzhou, Sichuan 646000, China.

International journal of biological macromolecules

|October 29, 2024

概括

工程纳米酶通过恢复氧化平衡和阻止炎症反循环来向动脉样硬化中的炎症. 这种方法减少了巨细胞的激活,并抑制了斑块的进展,提供了一种新的治疗策略.

科学领域:

生物材料科学生物材料科学
纳米技术纳米技术
心血管研究研究心血管研究

背景情况:

动脉样硬化 (AS) 涉及到动脉样硬化斑块内的超氧化离子 (O2-) 和过氧化 (H2O2) 等反应性氧物种 (ROS) 的代谢失调.
这种失调激活了涉及IL-1β,TNF-α和MCP-1的炎症反循环,加剧了巨细胞和血管光滑肌细胞 (VSMC) 之间的炎症.

研究的目的:

开发一种新型的氏丁硫酸盐 (CS) 功能化的双向工程纳米酶,用于动脉样硬化治疗.
研究纳米酶向炎症细胞和调节氧化应激和炎症通路的能力.

主要方法:

开发CS-Lip/PB@Rap,一种纳米酶,在CS修改的脂质体内封装装载有拉巴胺素 (Rap) 的中孔普鲁士蓝色纳米粒子 (PBs).
对CD44受体的CS功能化针对炎症性巨细胞和VSMCs.
评估纳米酶的类似酶的活动,氧化应激调节,以及对炎症信号通路 (例如NF-κB) 的影响.

主要成果:

CS-Lip/PB@Rap通过CD44受体向巨细胞和VSMC进行了有针对性的输送.
该纳米酶有效调节了氧化应激失衡,并抑制了NF-κB通路.
炎症反循环 (TNF-α,IL-1β,MCP-1) 被阻断,减少了炎症性巨细胞的产生和VSMC的表型切换.
减少氧化应激降低了氧化低密度脂蛋白 (ox-LDL),抑制泡细胞的形成和减轻动脉生成.

结论:

工程纳米酶可以有效地向动脉样硬化病变,并恢复ROS的代谢平衡.
这种纳米酶通过调节NF-κB通路来抑制巨细胞和VSMC之间的炎症交叉声.
开发的纳米酶通过减少氧化应激和炎症来缓解动脉样硬化进展,提供了一个有希望的策略.

关键词:

康德罗伊丁硫酸盐是功能化的纳米酶.炎症反循环的反循环是什么细胞间交叉通话是细胞间的交叉通话.

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