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Table 2 NMs inhibit RONS generation in neurological diseases

From: Nanomaterials alleviating redox stress in neurological diseases: mechanisms and applications

NMs

Disease models

Working mechanisms

Results

Refs.

Au NPs

AD

In vivo: Wistar male rats with an intracerebroventricular infusion of okadaic acid

By maintaining the normal mitochondrial function and inhibiting the neuroinflammation

Restore the spatial memory and cognition function

[126]

Au NPs

AD

In vitro: human embryonic stem cells cultured with Aβ1–42 synthetic peptide for 24 h

By improving the mitochondrial function

Rescue the Aβ-induced toxicity

[127]

Iron chelator loaded TAT-NFH-nBSA NPs

PD

In vivo: 10–11-week-old C57BL/6 male mice injected with MPTP

In vitro: SH-SY5Y cells cultured with MPTP

By delivering the non-Fe hemin-Cl for iron chelation

Reverse the parkinsonian symptoms

[145]

CeVO4 nanorods

In vitro: SH-SY5Y cells

By substituting the function of cytosolic SOD and mitochondrial SOD

Improve the cellular ATP levels and prevent the oxidative damage to neuronal cells

[157]

Pt NPs

PD

In vivo: < 8-month-old zebrafish injected with MPTP

By functioning as the mitochondrial complex I to alleviate the ROS generation

Increase the dopamine level and its metabolites and enhance the locomotor activity

[87]

  1. NPs: nanoparticles; AD: Alzheimer's disease; ROS: reactive oxygen species; PD: Parkinson’s disease; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Aβ: amyloid-β peptide; CeVO4: cerium vanadate; Pt: platinum