哈卡特
活性氧
氧化应激
透皮
化学
抗氧化剂
特应性皮炎
药理学
炎症
细胞因子
自愈水凝胶
药物输送
氧化铈
促炎细胞因子
羟基自由基
医学
人体皮肤
免疫系统
免疫学
氧化磷酸化
病变
细胞毒性
药品
作者
Thuy An Trinh,Ngoc Man Phan,Thanh Loc Nguyen,Jaeyun Kim
出处
期刊:Biomacromolecules
[American Chemical Society]
日期:2025-12-11
卷期号:27 (1): 121-133
标识
DOI:10.1021/acs.biomac.5c00741
摘要
Atopic dermatitis (AD) is a chronic inflammatory skin disorder driven by skin barrier dysfunction, immune dysregulation, a self-perpetuating cycle of inflammation and oxidative stress. Current therapies often target either oxidative stress or inflammation, yielding suboptimal outcomes. To overcome this, we developed Ce@iMyD88, a synergistic nanozyme, conjugating mesoporous cerium oxide nanoparticles with a MyD88 inhibitor (iMyD88), engineered to simultaneously scavenge reactive oxygen species (ROS) and suppress MyD88/NF-κB-mediated inflammatory signaling. Encapsulation in a lignin-based hydrogel provided biocompatibility, stability, and intrinsic antioxidant properties. In vitro, Ce@iMyD88 neutralizes superoxide, hydrogen peroxide, hydroxyl radicals, and attenuated ROS/proinflammatory cytokine expression in 2,4-dinitrochlorobenzene (DNCB)/H2O2-stimulated HaCaT keratinocytes. In vivo, applications in DNCB-induced AD and H2O2-challenged mice reduced epidermal thickness, mast cell infiltration, and restored skin barrier integrity. Compared with monotherapies, Ce@iMyD88 hydrogels markedly alleviated oxidative stress and inhibited MyD88/NF-κB signaling, reducing lesion severity and providing a precise strategy for managing inflammatory skin diseases through integrated nanoscale interventions.
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