ROS‐Response Nanoparticles for Edaravone Delivery: Pathological‐Activated Neuroprotection Against Ischemic‐Reperfusion Injury in Ischemic Stroke

Jul 8, 2025Advanced healthcare materials

Nanoparticles Delivering Edaravone for Targeted Brain Protection Against Stroke Damage

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Longevity & Aging on OpenScience ↗PubMed ↗DOI ↗

Abstract

A novel nanoparticle system, edaravone-loaded DEX-CDIPBE (DEX-CDIPBE-ED), demonstrates enhanced neuroprotective effects in ischemic stroke models.

DEX-CDIPBE-ED selectively releases edaravone in the ischemic penumbra during reperfusion, targeting oxidative stress.
This nanoparticle system exhibits potent antioxidant and neuroprotective effects in neuronal cells during ischemic and reperfusion phases.
In experiments with middle cerebral artery occlusion/reperfusion-treated rats, DEX-CDIPBE-ED prevents behavioral deficits more effectively than edaravone.
DEX-CDIPBE-ED reduces oxidative stress and inhibits neuroinflammation in the ischemic penumbra.
The findings suggest that DEX-CDIPBE-ED may provide a safer and more effective treatment for ischemic stroke.

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Ischemic stroke is a leading cause of mortality and disability, with ischemia-reperfusion injury exacerbating neuronal damage and neuroinflammation due to pathologically activated reactive oxygen species (ROS) production in the ischemic penumbra. Edaravone, a free radical scavenger, is approved for the clinical treatment of ischemic stroke. However, edaravone directly decreases ROS even at low concentrations, which may inhibit the physiological effects of ROS and largely limit the clinical application of edaravone. To overcome this challenge, a ROS-response nanoparticle system, edaravone-loaded DEX-CDIPBE (DEX-CDIPBE-ED), is developed for the selectively releasing edaravone in the ischemic penumbra during reperfusion, mitigating oxidative stress while minimizing off-target effects. DEX-CDIPBE-ED produces potent antioxidant and neuroprotective effects in neuronal cells mimicking ischemic and/or reperfusion phases of ischemic stroke. DEX-CDIPBE-ED further prevents behavioral deficits, reduces oxidative stress, and inhibites neuroinflammation with a higher potency than edaravone in the ischemic penumbra in middle cerebral artery occlusion/reperfusion (MCAO/R)-treated rats. These findings highlight the potential of DEX-CDIPBE-ED as a pathological activated antioxidative therapy for ischemic stroke, offering enhanced neuroprotection and reduced systemic toxicity.

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ROS‐Response Nanoparticles for Edaravone Delivery: Pathological‐Activated Neuroprotection Against Ischemic‐Reperfusion Injury in Ischemic Stroke

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