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] |
CeVO4Â 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] |