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<p>Baicalin (BA) is an active component of the natural plant <i>Scutellaria baicalensis</i>, which has been used over many years to treat inflammation and respiratory infections. In this study, the sepsis-induced acute lung injury (ALI) mouse model, network pharmacology and molecular docking were used to predict and explore the potential targets and signaling pathways of BA against ALI. The results showed that BA inhibited the major characteristics of ALI, including pathological changes, alveolar-capillary barrier dysfunction, increased inflammatory response and M1 macrophage polarization. Based on network pharmacology and molecular docking analyses, the PI3K/AKT/NF-κB pathway might be an important mechanism by which BA mitigated sepsis-induced ALI. Moreover, BA attenuated the phosphorylation of PI3K, AKT, IκB and NF-κB in the lung tissues of the ALI mice. In conclusion, this study demonstrated that BA ameliorated lung injury in mice, and depressed M1 macrophage polarization through inhibition of the PI3K/AKT/NF-κB pathway.</p>

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Exploring the effect and mechanism of baicalin on sepsis-induced acute lung injury based on network pharmacology and experimental verification

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月25日

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  • Pengwei Wang,
  • Ru Zhang,
  • Miaomiao Liu,
  • Jianlian Gao,
  • Yongheng Zhang,
  • Xiaohong Liu,
  • Caixia Li,
  • Yuanyuan Zhao,
  • Tiantian Zhu,
  • Xinghua Zhao,
  • Zhijian Deng

摘要

Baicalin (BA) is an active component of the natural plant Scutellaria baicalensis, which has been used over many years to treat inflammation and respiratory infections. In this study, the sepsis-induced acute lung injury (ALI) mouse model, network pharmacology and molecular docking were used to predict and explore the potential targets and signaling pathways of BA against ALI. The results showed that BA inhibited the major characteristics of ALI, including pathological changes, alveolar-capillary barrier dysfunction, increased inflammatory response and M1 macrophage polarization. Based on network pharmacology and molecular docking analyses, the PI3K/AKT/NF-κB pathway might be an important mechanism by which BA mitigated sepsis-induced ALI. Moreover, BA attenuated the phosphorylation of PI3K, AKT, IκB and NF-κB in the lung tissues of the ALI mice. In conclusion, this study demonstrated that BA ameliorated lung injury in mice, and depressed M1 macrophage polarization through inhibition of the PI3K/AKT/NF-κB pathway.