Vanadium Carbide Quantum Dots Exert Efficient Anti‐Inflammatory Effects in Lipopolysaccharide‐Induced BV2 Microglia and Mice

Abstract

The regulation of glial cell activation is a critical step for the treatment or prevention of neuroinflammation‐based brain diseases. However, the development of therapeutic drugs that pass the blood–brain barrier (BBB) and inhibit the glia cell activation remains a significant challenge. Herein, an ultrasmall 2D vanadium carbide quantum dots (V2C QDs) that are capable of crossing the BBB are prepared, and the admirable anti‐neuroinflammatory effects are presented. The prepared 2D V2C QDs with an average size of 2.54 nm show good hydrophilicity, physiological stability, and effective BBB‐crossing ability. The biological effect of V2C QDs on inflammatory reactions demonstrates fascinating results in preventing the impairment of learning and memory in BALB/c mice stimulated by lipopolysaccharide. Investigation of molecular mechanism reveals that V2C QDs not only inhibit the toll‐like receptor 4/myeloid differentiation factor 88‐mediated nuclear factor kappa B and mitogen‐activated protein kinase pathways, but also prevent eukaryotic translation initiation factor 2α/activating transcription factor 4/C/EBP homologous protein‐signaling pathway and reduce oxidative stress via activating the NF‐E2‐related factor‐2/heme oxygenase‐1‐signaling pathway, leading to greatly inhibited activation of microglia and astrocytes and weakened production of inflammatory cytokines. In summary, V2C QDs exert potent anti‐inflammatory effects through multiple pathways, thus offer great potential for the treatment of neurodegenerative diseases.

Keywords

• anti‐neuroinflammations
• blood–brain barrier permeabilities
• endoplasmic reticulum stress
• oxidative stress
• vanadium carbide quantum dots