# Proanthocyanidins carbon dots inhibit PRRSV infection by activating Nrf2/ARE to regulate oxidative stress and NLRP3 inflammasome-mediated pyroptosis

## TL;DR

Researchers developed proanthocyanidin-based carbon dots that inhibit PRRSV infection by reducing oxidative stress and inflammation in pig cells.

## Contribution

The study introduces proanthocyanidin-based carbon dots as a novel antiviral strategy targeting oxidative stress and NLRP3 inflammasome pathways in PRRSV.

## Key findings

- PAC-CDs significantly suppressed PRRSV replication in Marc-145 and PAM cells.
- PAC-CDs reduced NLRP3 inflammasome-mediated pyroptosis and pro-inflammatory cytokine release.
- PAC-CDs activated the Nrf2/ARE pathway to upregulate antioxidant defenses.

## Abstract

Carbon-derived nanomaterials, especially carbon dots (CDs), are gaining attention for their distinct physicochemical characteristics and broad-spectrum antiviral capabilities. However, their efficacy against economically critical pathogens like porcine reproductive and respiratory syndrome virus (PRRSV), a major threat to swine health-and the molecular pathways involved remain underexplored. Here, we developed innovative proanthocyanidin-based carbon dots (PAC-CDs) to enhance their antiviral efficacy against PRRSV by targeting oxidative stress pathways and suppressing NLRP3 inflammasome-mediated pyroptosis via activation of the Nrf2/ARE antioxidant axis. PAC-CD were synthesized as uniformly dispersed spherical nanostructures averaging 5.49 nm in diameter, exhibiting exceptional aqueous solubility and biocompatibility. These nanoparticles significantly suppressed PRRSV replication in both Marc-145 and porcine alveolar macrophage (PAM) cells, while mitigating infection-induced cytopathic damage. Mechanistically, PAC-CDs exert their antiviral effects not through direct viral neutralization but by hindering viral entry and replication via Nrf2 pathway activation, which upregulates antioxidant defenses and reduces oxidative damage. Consistently, PAC-CDs impaired PRRSV-induced NLRP3 inflammasome-triggered pyroptotic cell death and downstream pro-inflammatory cytokine release. These findings advance the development of targeted antiviral therapies and highlight the translational potential of PAC-CDs against PRRSV outbreaks, offering a dual-action strategy to alleviate oxidative injury and inflammatory cascades in infected hosts.

The online version contains supplementary material available at 10.1186/s13567-025-01642-5.