Scholarlink

Background <p>Enteroviruses (EVs), particularly types A (e.g., EV-A71) and B (e.g., CVB3), cause severe complications in vulnerable populations. Limited vaccines and no antivirals underscore the need for broad-spectrum therapies. Punicalagin, a natural anti-inflammatory compound, was investigated for its pan-enteroviral therapeutic potential.</p> Objective <p>To evaluate punicalagin’s efficacy and mechanisms against multiple EV serotypes via integrated systems pharmacology and experimental validation.</p> Methods <p>Network pharmacology identified punicalagin’s targets and pathways. In vitro antiviral activity was assessed in Vero/A549 cells infected with EV-A71/CVB3. Neonatal mice were intraperitoneally inoculated with these viruses to test in vivo efficacy. Molecular docking, apoptosis assays, and inflammatory factor analyses elucidated mechanisms.</p> Results <p>Punicalagin inhibited EV-A71 and CVB3 replication in <i>vitro</i> and improved survival in infected mice. Systems pharmacology linked its effects to anti-apoptotic and anti-inflammatory pathways. Molecular docking confirmed interactions with apoptosis/inflammation regulators (e.g., CASP3, TNF-α). Experimental validation demonstrated reduced viral-induced apoptosis and suppressed IL-6/TNF-α levels.</p> Conclusion <p>Punicalagin exhibits broad-spectrum anti-enteroviral activity through dual inhibition of apoptosis and inflammation, validated across in vitro, in vivo, and computational models. This study provides a systems-level framework for repurposing natural compounds against phylogenetically diverse EVs, addressing critical therapeutic gaps for high-risk populations.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Mechanism research of Punicalagin in treating representative strains of enterovirus A and B types based on systems pharmacology and experimental validation

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年7月9日

查看全文
  • Yuwei Liu,
  • Jing Chen,
  • Nana Du,
  • Min Zhao,
  • Yi Zhao,
  • Ping Wu,
  • Likai Ji,
  • Shixing Yang,
  • Xiaochun Wang,
  • Quan Shen,
  • Xiaodan Zhang,
  • Songyi Ning,
  • Hongfeng Yang,
  • Wen Zhang

摘要

Background

Enteroviruses (EVs), particularly types A (e.g., EV-A71) and B (e.g., CVB3), cause severe complications in vulnerable populations. Limited vaccines and no antivirals underscore the need for broad-spectrum therapies. Punicalagin, a natural anti-inflammatory compound, was investigated for its pan-enteroviral therapeutic potential.

Objective

To evaluate punicalagin’s efficacy and mechanisms against multiple EV serotypes via integrated systems pharmacology and experimental validation.

Methods

Network pharmacology identified punicalagin’s targets and pathways. In vitro antiviral activity was assessed in Vero/A549 cells infected with EV-A71/CVB3. Neonatal mice were intraperitoneally inoculated with these viruses to test in vivo efficacy. Molecular docking, apoptosis assays, and inflammatory factor analyses elucidated mechanisms.

Results

Punicalagin inhibited EV-A71 and CVB3 replication in vitro and improved survival in infected mice. Systems pharmacology linked its effects to anti-apoptotic and anti-inflammatory pathways. Molecular docking confirmed interactions with apoptosis/inflammation regulators (e.g., CASP3, TNF-α). Experimental validation demonstrated reduced viral-induced apoptosis and suppressed IL-6/TNF-α levels.

Conclusion

Punicalagin exhibits broad-spectrum anti-enteroviral activity through dual inhibition of apoptosis and inflammation, validated across in vitro, in vivo, and computational models. This study provides a systems-level framework for repurposing natural compounds against phylogenetically diverse EVs, addressing critical therapeutic gaps for high-risk populations.