ABSTRACT Acute kidney injury (AKI) is a fatal clinical syndrome primarily induced by aggravated oxidative stress, mitochondrial dysfunction, and renal tubular epithelial cell apoptosis. To tackle this challenge, we engineered an FA‐modified and redox‐sensitive chitosan (CS) nanocarrier delivery system for co‐delivery of NAC and CUR. These bio‐mimicked nanoparticles (165 nm, +28 mV) demonstrated enhanced colloidal stability, potent and consistent drug loading, and ROS‐sensitive release. When tested in H 2 O 2 ‐injured HK‐2 cells, the NAC‐ and CUR‐loaded NPs excelled in both powerfully reviving cell viability and intensely decreasing intracellular ROS and malondialdehyde levels. Not even the antioxidant defense markers such as the superoxide dismutase activity and GSH/GSSG ratio had definitively improved. This treatment precluded caspase‐3, ‐8, and ‐9, indicators of apoptosis. Gene expression validated increased Nrf2, HO‐1, and BCL‐2 and decreased BAX, KIM‐1, and NGAL, highlighting the system's multifunctional antioxidant and cytoprotective effects. These results confirm this nanoparticle platform as an enticing strategy to salvage redox homeostasis and shield renal tubular cells from oxidative injury with translational relevance in AKI treatment.
Xue et al. (Thu,) studied this question.
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