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<p>Baicalein (BAI), a phenolic flavonoid widely used in East Asian countries, is protective in various fibrotic and inflammatory diseases. This research aimed to determine the function of BAI and the specific mechanism by which it contributes to lipopolysaccharide (LPS)-induced lung inflammation in mice. Intratracheal injection of LPS produced inflammation in the lungs of the mice. The lung injury was assessed pathologically. Bronchoalveolar lavage and lung tissue were obtained to cells, quantify inflammatory cell counts, and total protein content. The zymography approach measured metalloproteinase activity. After neutrophil depletion in mice, the DCFH fluorescence assay was used to measure reactive oxygen species (ROS) formation. The tetramethyl benzidine oxidation technique was used to evaluate the activity of myeloperoxidase (MPO).&#xa0;The lung damage and the number of positive cells in the BAI-treated groups showed considerable improvement compared to the LPS group in mice with LPS-induced lung inflammation. Our investigation revealed that BAI decreased the total cell count and neutrophil count in the bronchoalveolar lavage fluid (BALF) after LPS treatment. Additionally, it suppressed the excessive production of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) in the bronchoalveolar lavage fluid (BALF). Moreover, BAI decreased MPO activity, and LPS activated ROS production in BALF cells via the TLR4/NF-κB pathway. The findings of our study demonstrate that BAI successfully reduced LPS-induced pulmonary edema, neutrophil infiltration, proinflammatory cytokine generation, and oxidative stress via the TLR4/NF-κB pathway.</p>

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Baicalein inhibits human neutrophil myeloperoxidase and protects mice from LPS-induced lung inflammation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月21日

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  • Chunyu Wei,
  • Jin Shang,
  • Na Gao,
  • Guocheng Zhang,
  • Jing Chang,
  • Qian Bai,
  • Yile Kou,
  • Hui Ding

摘要

Baicalein (BAI), a phenolic flavonoid widely used in East Asian countries, is protective in various fibrotic and inflammatory diseases. This research aimed to determine the function of BAI and the specific mechanism by which it contributes to lipopolysaccharide (LPS)-induced lung inflammation in mice. Intratracheal injection of LPS produced inflammation in the lungs of the mice. The lung injury was assessed pathologically. Bronchoalveolar lavage and lung tissue were obtained to cells, quantify inflammatory cell counts, and total protein content. The zymography approach measured metalloproteinase activity. After neutrophil depletion in mice, the DCFH fluorescence assay was used to measure reactive oxygen species (ROS) formation. The tetramethyl benzidine oxidation technique was used to evaluate the activity of myeloperoxidase (MPO). The lung damage and the number of positive cells in the BAI-treated groups showed considerable improvement compared to the LPS group in mice with LPS-induced lung inflammation. Our investigation revealed that BAI decreased the total cell count and neutrophil count in the bronchoalveolar lavage fluid (BALF) after LPS treatment. Additionally, it suppressed the excessive production of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) in the bronchoalveolar lavage fluid (BALF). Moreover, BAI decreased MPO activity, and LPS activated ROS production in BALF cells via the TLR4/NF-κB pathway. The findings of our study demonstrate that BAI successfully reduced LPS-induced pulmonary edema, neutrophil infiltration, proinflammatory cytokine generation, and oxidative stress via the TLR4/NF-κB pathway.