# Rhynchophylline attenuates porcine pseudorabies virus-induced astrocyte injury by modulating oxidative stress, inflammation, and metabolic abnormalities

**Authors:** Xiaoyu Liu, Yalong Sun, Jiajia Wei, Chen Guan, Weiyi Yang, Jianqin Li, Shengjia Sun, Xue Zhang, Xianghua Shu, Huayi Bai, Ying Zhang, Deng Pan, Chunlian Song

PMC · DOI: 10.3389/fphar.2026.1782776 · Frontiers in Pharmacology · 2026-03-16

## TL;DR

Rhynchophylline protects brain cells from a virus by reducing oxidative stress, inflammation, and metabolic issues in a lab study.

## Contribution

This study is the first to show RHY's protective effects against PRV-induced astrocyte injury through multiple mechanisms.

## Key findings

- RHY reduced PRV replication and oxidative stress markers in infected cells.
- RHY suppressed pro-inflammatory cytokines and enhanced anti-inflammatory ones.
- RHY restored metabolic pathways disrupted by PRV infection.

## Abstract

Porcine pseudorabies virus (PRV) causes astrocyte injury through oxidative stress, inflammatory responses, and metabolic dysfunction. Rhynchophylline (RHY) possesses antioxidant and anti-inflammatory properties, but its protective effects against PRV infection remain unclear. Using PRV-infected C8-D1A cells, we evaluated the antiviral and cytoprotective effects of RHY. At a non-toxic concentration of 5 μM, RHY significantly inhibited PRV replication, reduced intracellular reactive oxygen species, and alleviated oxidative stress by decreasing xanthine oxidase (XOD), myeloperoxidase (MPO), malondialdehyde (MDA), and nitric oxide (NO) levels while restoring superoxide dismutase (SOD) activity. RHY also modulated PRV-induced inflammatory imbalance by suppressing interleukin (IL)-6 and IL-8 and enhancing IL-4 and IL-10 expression. Metabolomic profiling revealed that PRV infection disrupted cellular metabolism, particularly pathways related to unsaturated fatty acid biosynthesis and the tricarboxylic acid (TCA) cycle, which were largely restored by RHY treatment. These findings indicate that RHY exerts antiviral, anti-inflammatory, and antioxidant effects by correcting PRV-induced metabolic disturbances in vitro.

## Linked entities

- **Chemicals:** Rhynchophylline (PubChem CID 5281408), malondialdehyde (PubChem CID 10964), nitric oxide (PubChem CID 145068)
- **Species:** Sus scrofa (taxon 9823)

## Full-text entities

- **Genes:** IL4 (interleukin 4) [NCBI Gene 3565] {aka BCGF-1, BCGF1, BSF-1, BSF1, IL-4}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, SOD1 (superoxide dismutase 1) [NCBI Gene 6647] {aka ALS, ALS1, HEL-S-44, IPOA, SOD, STAHP}, MPO (myeloperoxidase) [NCBI Gene 4353], IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}
- **Diseases:** metabolic abnormalities (MESH:D008659), astrocyte injury (MESH:D001254), metabolic disturbances (MESH:D024821), inflammation (MESH:D007249)
- **Chemicals:** RHY (MESH:C052714), reactive oxygen species (MESH:D017382), unsaturated fatty acid (MESH:D005231), NO (MESH:D009569), TCA (MESH:D014233), MDA (MESH:D008315)

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13033685/full.md

## References

38 references — full list in the complete paper: https://tomesphere.com/paper/PMC13033685/full.md

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Source: https://tomesphere.com/paper/PMC13033685