Rosmarinic acid inhibits lung injury induced by diesel exhaust particles

Chiaki Sanbongi, Hirohisa Takano, Naomi Osakabe, Naoko Sasa, Midori Natsume, Rie Yanagisawa, Ken Ichiro Inoue, Yoji Kato, Toshihiko Osawa, Toshikazu Yoshikawa

Research output: Contribution to journalArticlepeer-review

101 Citations (Scopus)


Epidemiological and experimental studies have suggested that diesel exhaust particles (DEP) may be involved in recent increases in lung diseases. DEP has been shown to generate reactive oxygen species. Intratracheal instillation of DEP induces lung inflammation and edema in mice. Rosmarinic acid is a naturally occurring polyphenol with antioxidative and anti-inflammatory activities. We investigated the effects of rosmarinic acid on lung injury induced by intratracheal administration of DEP (500 μg/body) in mice. Oral supplementation with administration of rosmarinic acid (2 mg/body for 3 d) inhibited DEP-induced lung injury, which was characterized by neutrophil sequestration and interstitial edema. DEP enhanced the lung expression of keratinocyte chemoattractant (KC), interleukin-1β, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1α, which was inhibited by treatment with rosmarinic acid. DEP enhanced expression of iNOS mRNA and formation of nitrotyrosine and 8-OHdG in the lung, which was also inhibited by rosmarinic acid. These results suggest that rosmarinic acid inhibits DEP-induced lung injury by the reduction of proinflammatory molecule expression. Antioxidative activities of rosmarinic acid may also contribute to its protective effects.

Original languageEnglish
Pages (from-to)1060-1069
Number of pages10
JournalFree Radical Biology and Medicine
Issue number8
Publication statusPublished - 2003 Apr 15
Externally publishedYes


  • Diesel exhaust particles
  • Free radicals
  • Lung injury
  • Reactive oxygen species
  • Rosmarinic acid

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)


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