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Innovative Medicines & Omics Antioxidant nanomedicines for therapies

Table 2. Summary of representative antioxidant nanomedicines for the treatment of bone diseases.
Antioxidant nanomedicine Reaction type Disease References
DNA origami nanostructure Non-catalytic Rheumatoid arthritis 158
Mg nanoparticle Non-catalytic Rheumatoid arthritis 159
CeO nanoparticle-loading MSN Catalytic Rheumatoid arthritis 162
2
Tannic acid-Fe network Catalytic Rheumatoid arthritis 165
Mn porphyrin-based biomimetic nanosheet Catalytic Rheumatoid arthritis 166
Porphyrin-loading Mn-doped hollow MSN Catalytic Rheumatoid arthritis 170
SOD-loading polymersome Catalytic Osteoarthritis 180
Catalase-loading ZIF-8 nanoparticle Catalytic Osteoarthritis 181
L-dopa-based nanoparticle Non-catalytic Osteoarthritis 182
Black phosphorus nanosheet Non-catalytic Osteoarthritis 184
MnO nanoparticle Catalytic Osteoarthritis 185
2
Prussian blue nanoparticle Catalytic Osteoporosis 194
Abbreviations: MSN: Mesoporous silica nanoparticles; SOD: Superoxide dismutase; ZIF-8: Zeolitic imidazolate framework-8

took advantage of the catalytic hydrogenation effect of Pd of Alzheimer’s disease, being a competent candidate for
nanoparticles, to carry antioxidant gas H for scavenging treating this disease.
2
intracranial ROS. As the mitochondrial bioenergetic
212
deficit is the key pathology of Alzheimer’s disease, 5.2. Parkinson’s disease treatment
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Recently, Qian et al. constructed poly(trimethylene Different from Alzheimer’s disease, Parkinson’s disease is
carbonate)-based nanoparticles for loading an antioxidant characteristic of dopaminergic neuron loss in substantia
peptide SS31 to remove mitochondrial ROS of cholinergic nigra pars compacta, which results in symptoms of
neurons (Figure 12). The nanoparticle can penetrate uncontrollable tremor and slowness of movement. The
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BBB and enter cholinergic neurons under the assistance pathology of Parkinson’s disease is closely associated
of a surface-modified peptide, then the SS31 with intrinsic with the redox chemistry of dopamine. This amino-
mitochondria-targeting property favors antioxidation group armed catechol can coordinate Fe and reduce
3+
reaction specifically in mitochondrial region, normalizing its oxidation state to initiate pro-oxidant reactions
mitochondrial bioenergetics and alleviating the symptoms producing H O , during which neuromelanin is
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2
2
of Alzheimer’s disease. formed, which can further coordinate Fe to trigger
3+
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Inorganic antioxidant nanocatalysts, such as pro-oxidant reactions. The generated H O can be
2
2
CeO nanoparticles, have also been used for catalytic converted into highly oxidizing •OH through Fenton
2
antioxidation therapy of Alzheimer’s disease. A follow-up reactions, resulting in oxidative stress and inflammation,
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study further demonstrated that CeO could promote the and leading to the aggregation and deposition of
2
shift of microglia polarization from a pro-inflammatory α-synuclein, which further restrains dopamine
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M1 phenotype to an anti-inflammatory M2 phenotype, synthesis. For the treatment of Parkinson’s disease, the
favoring the regulation of immune microenvironment. FDA-approved drug amantadine hydrochloride can only
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This antioxidant nanocatalyst has also been engineered promote dopamine synthesis in the striatum, but fails
in MSN-based drug delivery system for combinational to address oxidative stress or the upstream metal ion-
therapy of Alzheimer’s disease by antioxidation and triggered pro-oxidant reactions.
Tau phosphorylation inhibition. Cai et al. prepared Inorganic antioxidant nanocatalysts have been applied
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manganese hexacyanoferrate nanoparticles that can in the treatment of Parkinson’s disease. CeO nanoparticles
2
not only scavenge ROS to mitigate neuroinflammation, were demonstrated to inhibit microglial activation and lipid
but also inhibit Tau hyperphosphorylation. Gao et al. peroxidation by scavenging ROS, and protect the tyrosine
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demonstrated that polyoxometalate (POM) nanoparticles hydroxylase in the strata as well. Hao et al. constructed
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can present SOD-like activity for ROS scavenging, porous Cu O nanoparticles possessing SOD, catalase,
x
protease-like activity for clearing Aβ aggregates, and and GSH peroxidase-like activities, capable of alleviating
metal-chelating activity for maintaining Cu homeostasis. oxidative stress to rescue memory loss of mice with
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This nanomaterial addresses multiple pathogenic factors Parkinson’s disease. As microglia is a kind of important
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Volume 1 Issue 1 (2024) 16 doi: 10.36922/imo.2527