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<p>Since COVID-19 pandemic, the protection of lung health against infection with various pathogens has been emphasized. Acute lung injury (ALI) is a severe respiratory disease that causes sudden loss of lung function via pathogenic invasion. Although diverse anti-inflammatory materials have been investigated, the preventive efficacy remains limited. The purpose of this study is to investigate the preventive effects of <i>Melicope pahangenesis</i> T. G. Hartley extract (MPE) on lipopolysaccharide (LPS)-induced ALI. In vivo, oral MPE administration inhibits LPS-induced intestinal thickening, hyperplasia, mucus production, alveolar macrophage recruitment, and IL-1β expression in bronchoalveolar lavage fluid. The production of IL-6 and expression of iNOS and COX-2 were strongly suppressed. In mechanism studies, MPE inhibited phosphorylation of p65, IκB kinase, p38, and JNK1/2 and nuclear translocation of p65. Furthermore, MPE reduced reactive oxygen species and induced radical scavenging activities. Taken together, MPE consistently exerted anti-inflammatory effects in vitro and in vivo.</p>

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The inhibitory effects of Melicope pahangenesis T. G. Hartley extract on LPS-induced acute lung injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月10日

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  • Hee Jung Choi,
  • Min Jeong Kim,
  • Jin Hyub Paik,
  • Dong Joon Kim,
  • Sung Keun Jung

摘要

Since COVID-19 pandemic, the protection of lung health against infection with various pathogens has been emphasized. Acute lung injury (ALI) is a severe respiratory disease that causes sudden loss of lung function via pathogenic invasion. Although diverse anti-inflammatory materials have been investigated, the preventive efficacy remains limited. The purpose of this study is to investigate the preventive effects of Melicope pahangenesis T. G. Hartley extract (MPE) on lipopolysaccharide (LPS)-induced ALI. In vivo, oral MPE administration inhibits LPS-induced intestinal thickening, hyperplasia, mucus production, alveolar macrophage recruitment, and IL-1β expression in bronchoalveolar lavage fluid. The production of IL-6 and expression of iNOS and COX-2 were strongly suppressed. In mechanism studies, MPE inhibited phosphorylation of p65, IκB kinase, p38, and JNK1/2 and nuclear translocation of p65. Furthermore, MPE reduced reactive oxygen species and induced radical scavenging activities. Taken together, MPE consistently exerted anti-inflammatory effects in vitro and in vivo.