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Innovative Medicines & Omics Antioxidant nanomedicines for therapies

property and used for alleviating neuroinflammation in efficiently. Li et al. used POM nanoparticles for mitigating
Parkinson’s disease. 230 cerebral ischemia-reperfusion injury through intrathecal
Mitophagy is an autophagic process specific for injection, which allows nanocatalysts to directly enter
damaged mitochondria, maintaining the functional pool cerebrospinal fluid and bypass BBB to reach ischemic
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of respiring mitochondria. 231,232 Therefore, activating penumbra, favoring therapeutics.
mitophagy enables timely clearance of damaged In the whole process of stroke treatment, the
mitochondria in dopaminergic neurons under oxidative combination of thrombolysis and antioxidation is proposed
stress. Very recently, Li et al. have constructed a CeO to achieve both blood supply restoration and alleviation
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nanocatalyst atomically dispersed with Pt species, which of subsequent ischemia-reperfusion injury. Very recently,
can not only scavenge ROS efficiently, but also induce Wang et al. prepared a kind of self-assembled polypeptide
mitophagy by electrostatic adsorption, synergistically nanoparticle and used it to template MnO growth in the
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elevating the therapeutic outcome of Parkinson’s disease core (Figure 15). The polypeptide shell with multiple
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(Figure 13). 233 components can not only target thrombus to recanalize
vessel occlusion, but also penetrate BBB and further target
5.3. Ischemic stroke treatment stroke neuron. Importantly, the nanoparticle presents SOD
Ischemic stroke is caused by cerebral embolism that blocks and catalase-like activities that can scavenge cellular ROS
blood flow in brain. The FDA-approved thrombolytic efficiently, protecting neurons from ischemia-reperfusion
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tPA is often used in ischemic lesions for thrombolysis and injury. This work addresses both thrombus and ischemia-
restoring blood supply. However, during reperfusion, reperfusion injury of ischemic stroke, providing a
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a large amount of ROS is generated inevitably, leading to feasible strategy for synergistically normalizing the
a severe ischemia-reperfusion injury. The antioxidant microenvironment of brain.
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edaravone has been used to mitigate oxidative damage
in ischemic stroke treatment. However, its further 5.4. Traumatic brain injury treatment
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clinical application suffers from a short half-life, low Brain trauma triggered by accidents can cause primary and
bioavailability, low BBB penetrability, and toxicity to secondary phases of brain injury. Primary brain injury
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kidney and liver. 238 caused by external force can further trigger a biochemical
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The development of antioxidant nanomedicines has cascade including ROS production, leading to a long-
provided feasible strategies to improve the therapeutic lasting secondary injury such as neuroinflammation and
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outcome of ischemic stroke. He et al. prepared a poly(2- brain edema. Timely scavenging of ROS is important to
diisopropyl methacrylate)-based nanocarrier and used mitigate secondary injury. However, no antioxidant drug
it to load succinobucol antioxidant for ischemic stroke has hitherto been approved for treating traumatic brain
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therapy (Figure 14). Based on the intrinsic BBB- injury.
penetrating ability of 4T1 cancer cells, the nanomedicine It was reported that nanoparticles can accumulate in
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was further modified with 4T1 cell membrane, enabling brain injury region passively through EPR effect, due to
their accumulation in cerebral ischemic lesions. After the traumatic damage of BBB. Therefore, antioxidation
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internalization by various cells in brain, the nanocarrier nanomedicines can accumulate at pathological sites to
can degrade to release succinobucol, which is favorable for protect brain from oxidative damage. Yoo et al. prepared a
mitigating ischemia-reperfusion injury. thioether-containing nanoparticle with antioxidative effect
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Nanomaterials with intrinsic antioxidative properties for reducing secondary brain injury. An early study also
have also been used in ischemic stroke treatment. Liu et al. used carbon particles to alleviate oxidative stress after brain
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used melanin nanoparticles to protect brain from oxidative trauma. Different from fullerene, which is an antioxidant
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damage in ischemic stroke. CeO nanoparticles have also catalyst, the carbon particle with graphitic structural
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2
been reported to be effective in alleviating the symptoms. domains can scavenge ROS though non-catalytic reaction,
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Our group reported an edaravone-loaded CeO during which each graphitic structural domain inactivates
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nanoparticle modified with Angiopep-2, which enables ROS by forming a C-O bond.
simultaneous BBB protection and antioxidant treatment of Antioxidant nanocatalysts have also been applied
stroke. He et al. utilized a solvothermal reaction to grow in alleviating traumatic brain injury. Mu et al. prepared
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ZIF-8 layer on CeO nanoparticles to improve their stability a trimetallic nanocatalyst that can mimic the activities
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•−
in physiological condition, as well as catalytic antioxidative of multiple antioxidases to scavenge O , H O and
2,
2
2
activities. The composite nanoparticle was evidenced •OH efficiently. In vivo experiments indicate that the
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to reverse reperfusion-induced injury in ischemic stroke nanocatalyst can mitigate neuroinflammation, improve
Volume 1 Issue 1 (2024) 18 doi: 10.36922/imo.2527