From: Nanomaterials alleviating redox stress in neurological diseases: mechanisms and applications
NMs | Characterization | Disease models | Treatment | Target RONS | Valence states | Working mechanism | Results | Refs. |
---|---|---|---|---|---|---|---|---|
Fe3O4 NPs | Size: 20 nm | AD In vivo: 6-week-old drosophila AD model In vitro: PC12 cells | 200 μg/mL, fed with food containing NPs | H2O2 | – | CAT-like activity for ROS scavenging | Diminish the α-Synuclein accumulation, enhance climbing ability and prolong life span of animals | [34] |
Fe3O4 NPs | Size: 200 nm; Surface modification: rough surface with PEG | Ischemic stroke In vivo: 8-week-old male mice MACO models In vitro: PC12 cells | 15 and 50 mg/kg, orally administered | H2O2, ·OH, O2·− | – | CAT-, POD-, SOD-like activity for ROS scavenging and protecting the BBB integrity | Reduce cerebral infarct volume and improve the symptoms of neural dysfunction | [9] |
CeO2 NPs | Size: 10 nm | Ischemic stroke In vivo: hippocampal brain slice of 2 ~ 5-month-old CD1 mice | 0.1–2 μg/mL, added to the solution with brain slices | O2·−, ONOO−, ·NO | – | SOD-like activity for RONS scavenging | Reduce the area of ischemia-induced cell death | [51] |
CeO2 NPs | Size: ~ 3–8 nm | AD In vitro: cortical neurons cultured with Aβ peptide | 100 nM for 3 h | ONOO− | Ce3+ and Ce4+ | Scavenging ONOO− and reducing Aβ-induced mitochondrial fragmentation | Reduce the neuronal cell death | [54] |
CeO2 NPs | Size: ~ 20 ± 5 nm; Shape: polyhedral; Surface modification: ZIF-capped | Ischemic stroke In vivo: female SD mice MACO models In vitro: PC12 cells | 0.2 and 0.4 mg/kg, tail intravenously administered for 3 d | H2O2, ·OH, O2·− | Ce3+ and Ce4+ | ROS scavenging and anti-neuroinflammation | Block ischemic reperfusion damage and reduce the infarct volume | [28] |
CeO2 NPs | Size: 3 nm; Surface modification: aminocaproic acid | SAH In vivo: male SD rats SAH model In vitro: RAW264.7 | 0.5 mg/kg, intravenously administered at 1 h post-SAH | O2·− | Ce3+ and Ce4+ | ROS scavenging and anti-neuroinflammation | Reduce the neuronal death and the brain edema | [8] |
CeO2 NPs | Size: 4.3 ± 0.5 nm; Shape: spherical; Surface modification: Angiopep-2 and PEG | Ischemic stroke In vivo: SD rats MACO models In vitro: BCECs | 0.5 mg/kg, tail intravenously administered for 24 h | H2O2, ·OH, O2·−, ·NO | Ce3+ and Ce4+ | ROS scavenging and protecting BCECs | Prevent the BBB damage and reduce the infarct volume | [10] |
CeO2 NPs | Size: 3–4 nm; Shape: spherical; Surface modification: PEG | ICH In vivo: 8-week-old male SD rats ICH models In vitro: U937 and RAW264.7 cells | 0.5 mg/kg, intravenously administered for 6 and 30 h | H2O2, ·OH, O2·−, ONOO−, ·NO | Ce3+ and Ce4+ | RONS scavenging, anti-neuroinflammation and reducing microglia recruitment | Reduce the brain edema | [47] |
Cr-doped CeO2 NPs | Size: 8–12 nm | TBI In vivo: 8–10-week-old male C57BL/6 mice TBI models | Nanozyme patch adhered to the injured brain area for 2–28 d | H2O2, ·OH, O2·−, ONOO−, ·NO | Ce3+ and Ce4+ | RONS scavenging and anti-neuroinflammation | Reduce the neuronal cell death and promote wound healing | [48] |
CeO2 NPs | Size: 3, 11, 22Â nm; Surface modification: lipid, PEG, and TPP | PD In vivo: C57BL/6 mice injected with MPTP In vitro: SH-SY5Y and HeLa cells | 0.1 and 0.3Â mM, stereotactically administered for 7 d | - | Ce3+ and Ce4+ | Scavenging intracellular and/or mtROS and anti-neuroinflammation | Protect axons of dopaminergic neurons and reduce activation of microglia | [46] |
Single-atom Pt-CeO2 | CeO2 clusters doped Pt | TBI In vivo: male C57BL/6 mice TBI models In vitro: HT22 cells | Nanozyme bandage pasted on injured brain area for 12 and 26 d | ·OH, O2·−, ONOO−, ·NO | Ce3+ and Ce4+ | RONS scavenging and anti-neuroinflammation | Improve impaired neurocognition | [166] |
TPP-CeO2 NPs | Size: 22 nm; Surface modification: PEG and TPP | AD In vivo: 6-month-old 5XFAD transgenic mice AD models In vitro: SH-SY5Y cells | Stereotaxically administered for 7 d | H2O2, O2·− | Ce3+ and Ce4+ | Scavenging mtROS and inhibiting microglia activation | Mitigate the reactive gliosis and reduce the neuronal cell death | [45] |
CuO and Cu2O NP clusters | Size: 65 ± 7 nm; Surface modification: tyrosine, aspartic acid, glutamic acid, and phenylalanine | PD In vivo: 8–10-week-old male C57BL/6 mice injected with MPTP In vitro: SH-SY5Y cells cultured with MPP+ | 0.2 mg/mL, stereotaxically administered for 15 d | H2O2, ·OH, O2·− | – | CAT-, SOD-, POD-, and GPx- like activity for ROS scavenging | Promote the cognitive recovery and rescue the memory loss | [31] |
Mn3O4 NPs | Size: cubes: 50 nm, polyhedron: 60 nm, hexagonal plates: 140 nm, flakes-like morphology: 100 nm, and flower-like morphology: 180 nm | PD In vitro: SH-SY5Y cells cultured with MPP+ | 2.5, 5, 10, 20 ng/μL | H2O2, ·OH, O2·− | – | CAT-, SOD-, and GPx- like activity for ROS scavenging | Rescue the loss of neurites | [59] |
2D vanadium carbide MXenzyme | Lateral size: several micrometers; Shape: 2D nanoflakes | PD In vivo: 6-week-old female C57BL/6 mice injected with MPTP In vitro: L929 and PC12 cells | 10 mg/mL, 4 μL, unilaterally injected into the striatum | H2O2, ·OH, O2·− | V5+ and V4+ | CAT-, SOD-, POD-, and GPx-like activity for ROS scavenging, anti-neuroinflammation, and inhibiting microglia activation | Increase the TH levels and reduce the lipid peroxidation | [66] |
Mo-based POM nanoclusters | Size: ~ 1 nm | Ischemic stroke In vivo: MCAO rats In vitro: primary neurons | 1 μg/μL, 50 μL, intrathecally administered | H2O2, ·OH, O2·− | – | RONS scavenging and anti-neuroinflammation | Reduce the infarct volume and improve the neurological function | [77] |
MoS2 NPs | Size: ~ 100 nm; Shape: spherical | AD In vitro: SY5Y cells cultured with Aβ42 | 1, 5, 10 μg/mL for 12 h | – | – | ROS scavenging and inhibiting Aβ aggregation | Reduce the neuronal cell death | [76] |
CuxO@EM-K | Size: 90 ± 15 nm; Surface modification: DSPE-PEG | AD In vivo: 9-month-old female 3xTg-AD mice models | 15 mg Cu/kg, intravenously administered for 12, 24, 36, and 48 h | H2O2, O2·− | – | ROS scavenging and adsorbing Aβ | Reduce the Aβ burden in the blood and brain and ameliorate memory deficit | [73] |
Pt NPs | Size: 2–3 nm | Ischemic stroke In vivo: male C57/BL6 mice MACO models | 4.0 μM/kg, 0.3 mL, tail intravenously administered | O2·− | - | ROS scavenging | Reduce the infarct volume and improve motor function | [86] |
Pd hydride NPs | Size: ~ 30 nm; Shape: cubic | AD In vivo: male and female 5-month-old 3xTg-AD mice models In vitro: Neuro-2A and N2a-SW cells | 0.5, 1, and 2 mg/mL, 2 μL, bilateral intracerebral administered | ·OH | – | ROS scavenging and ameliorating the mitochondrial dysfunction | Ameliorate the cognitive impairment, reverse the synaptic deficits and neuronal death, and inhibit Aβ generation and aggregation | [88] |
PEG-HCCs | Size: 40 nm × 2 nm; Surface modification: PEG | Ischemic stroke In vivo: male SD MACO rat In vitro: B. End3 brain endothelial cells and E17 primary cortical neurons | 4 mg/kg, < 0.1 mL, tail intravenously administered | H2O2, ·OH, O2·− | – | ROS scavenging | Reduce the infarct volume, hemisphere swelling, and hemorrhage score, and improve neurological function | [94] |
Carboxyfullerene | – | PD In vivo: male macaque fascicularis monkey; MPTP-induced PD model; Age (years old): controls: 7.6 ± 2.2; experimental group: 8.1 ± 2.3 | 200 mg/mL, 3 mg/kg/day for 8 weeks, parenteral administered | – |  | Alleviating redox stress and anti-neuroinflammation | Reduce striatal injury, improved parkinsonian motor ratings, and increase the striatal dopamine levels | [7] |
Polyhydroxylated fullerene derivatives | – | Ischemic stroke In vivo: 10–12-week-old male Wistar rats, ischemia/reperfusion models | 1 mg/kg, 1 mL, intraperitoneally administered | – |  | Alleviating redox stress | Reduce the infarct volume and tissue swelling of ischemic hemispheres, and improve the neurological disabilities | [99] |
UCNP@C60-pep | Size: 30 nm; Surface modification: Aβ-target peptide KLVFF | AD In vivo: AD model CL2006 strain In vitro: PC12 cells | 100 µg/mL for 6 d | – | – | Alleviating redox stress and inhibiting Aβ aggregation | Prolong the lifespan of CL2006 strain | [101] |
Carbogenic nanozyme | Size: ~ 2.7 nm; Surface modification: hydroxy and amide/amino groups | TBI In vivo: 6–8-week-old male C57 BL/6 mice, TBI model In vitro: Neuro 2A cells | 5 mg/mL tail intravenously administered for 3.5 months | H2O2, ·OH, O2·−, ONOO−, ·NO | – | RONS scavenging and anti-neuroinflammation | Improve the spatial learning and memory abilities | [104] |
GOQDs | Lateral sizes: 20 ~ 40 nm | PD In vivo: larval zebrafish, MPP+-induced PD models In vitro: PC12 cells | 100 µg/mL | H2O2 | – | ROS scavenging and diminishing mitochondrial damage | Reduce the expression of α-synuclein and increase locomotive activity and Nissl bodies in the brain | [106] |
PEG-melanin NPs | Size: ~ 120 nm; Shape: spherical Surface modification: PEG | Ischemic stroke In vivo: male Wistar MACO rat model In vitro: Neuro 2A cells | 10 mg/mL, stereotaxically administered | H2O2, ·OH, O2·−, ONOO−, ·NO | – | RONS scavenging and anti-neuroinflammation | Reduce the infarct volume | [5] |
Hollow prussian blue NPs | Size: ~ 65 nm with an inner cavity | Ischemic stroke In vivo: SD rats MACO models In vitro: Raw264.7 and SH-SY5Y cells | 40 μg/mL, 10 μL, stereotaxically administered | H2O2, ·OH, O2·−, ONOO− | – | ROS scavenging and anti-neuroinflammation | Alleviate the cerebral metabolic impairment, reduce the infarct volume, and attenuate the neurological deficits | [113] |