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Innovative Medicines & Omics Antioxidant nanomedicines for therapies
A
B
Figure 11. (A and B) Schematic illustration of the synthetic procedures and anti-osteoarthritis mechanism of catalase-loading zeolitic imidazolate
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framework-8 nanoparticle. Reproduced with permission from Zhou et al. Copyright © 2019, American Chemical Society.
oxidative microenvironment of osteoporosis, consequently thus capable of penetrating BBB to trigger antioxidation
suppressing osteoclastogenesis and bone resorption, reactions in the brain.
and inhibiting osteoporotic bone loss. However, this
nanocatalyst cannot promote osteogenesis to restore the 5.1. Alzheimer’s disease treatment
density and function of bone tissue. It is expected that future Alzheimer’s disease is a main cause of age-related
works can address both osteoclast-based bone resorption dementia, which may lead to symptoms such as loss
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and osteoblast-based bone regeneration concurrently for of memory, cognitive decline, and even behavioral
synergistically restoring bone structure. and physical disability. The pathology of Alzheimer’s
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Current antioxidant nanomedicines for treating bone disease is associated with mitochondrial dysfunction that
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2+
diseases are mainly for arthritis treatment (Table 2). results in the overproduction of ROS. In addition, Cu
Recent studies reported that antioxidative nanomedicines accumulation and amyloid-β (Aβ) peptide deposition also
2+
can protect bone mesenchymal stem cells from oxidative occur. 204-206 Aβ can coordinate Cu , reducing its oxidation
stress to extend their fate, 195,196 which may provide new state to facilitate pro-oxidant reactions generating H O
2
2
approaches for treating other severe bone diseases that from O . 207-209 Fenton reactions then further convert H O
2
2
2
require transplantation of bone mesenchymal stem cells. into highly oxidizing •OH, leading to oxidative damage to
neurocytes. In addition, research shows that Tau protein
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5. Brain disease treatment hyperphosphorylation can also elevate mitochondrial
oxidative stress. Therefore, the scavenging of excessive
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Oxidative stress is involved in the pathological progresses ROS, the maintenance of Cu homeostasis, the clearance
of various brain diseases, such as neurodegenerative of Aβ, and the inhibition of tau phosphorylation are
diseases (Alzheimer’s disease and Parkinson’s disease),
ischemic stroke, and traumatic brain injury, during which strategies for treating Alzheimer’s disease. However, the
ROS will weaken the activity of neurocytes and lead to FDA-approved drug memantine can only target N-methyl-
apoptosis. Due to the existence of blood–brain barrier D-aspartate receptor, unable to address these pathogenic
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(BBB, a dynamic interface between blood and brain tissue factors.
that selectively impedes the passage of substances), the Various antioxidant nanomedicines have been
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antioxidant nanomedicines should be small enough, 198-200 engineered for treating Alzheimer’s disease. Zhang et al.
Volume 1 Issue 1 (2024) 15 doi: 10.36922/imo.2527

