ROS-Responsive Nanoparticles Mediate Rhein Release to Reprogram Macrophages for Attenuating Acute Kidney Injury

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https://storage.unitedwebnetwork.com/files/1099/42da6838eeaa65a0ca8ec0d0158cae9d.pdf

Abstract Title *

ROS-Responsive Nanoparticles Mediate Rhein Release to Reprogram Macrophages for Attenuating Acute Kidney Injury

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MEICEN WU u3626593@connect.hku.hk The University of Hong Kong School of Chinese Medicine Hong Kong China *

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Introduction

Acute Kidney Injury (AKI) is a critical condition affecting 10-15% of hospitalized patients globally (>50% in ICU) and 3-8% in China (>20% in ICU). The treatment of AKI faces challenges due to limited drug penetration caused by pathological barriers and charge selectivity. Rhein, a natural compound with potent anti-inflammatory effects targeting NF-κB pathways, is limited by poor solubility, low bioavailability, and hepatotoxicity with long-term use.

Methods

Rhein was encapsulated into amphiphilic hyaluronic acid-bilirubin conjugate via self-assembly (HA-BR@Rhein NPs). Morphological transformation of NPs under H₂O₂ was assessed using TEM. Biological evaluation included flow cytometry analysis of macrophage polarization and qPCR for inflammatory marker expression.

Results

Upon ROS exposure, HA-BR@Rhein NPs underwent a morphological transformation from spherical to nanorod, which consequently enhanced their retention time in renal. Flow cytometry analysis revealed that this formulation effectively promoted macrophage polarization towards the anti-inflammatory phenotype (CD206⁺/CD86⁻). This phenotypic shift was further corroborated by qPCR results, showing a substantial downregulation in the expression of key pro-inflammatory cytokines, including IL-6 and IL-1β, in AKI models.

Conclusion

ROS-responsive nanoparticles enable controlled Rhein release in juried kidney and effectively promote macrophages reprogramming towards an anti-inflammatory phenotype. This approach may serve as a potential therapeutic treatment for AKI.

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