Sanbongi Chiaki, Takano Hirohisa, Osakabe Naomi, Sasa Naoko, Natsume Midori, Yanagisawa Rie, Inoue Ken-ichiro, Kato Yoji, Osawa Toshihiko, Yoshikawa Toshikazu
Health and Bioscience Laboratories, Meiji Seika Kaisha, Ltd, Saitama, Japan.
Free Radic Biol Med. 2003 Apr 15;34(8):1060-9. doi: 10.1016/s0891-5849(03)00040-6.
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 microg/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-1beta, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1alpha, 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.
流行病学和实验研究表明，柴油废气颗粒（DEP）可能与近期肺部疾病的增加有关。已证明DEP可产生活性氧。气管内注入DEP可诱导小鼠肺部炎症和水肿。迷迭香酸是一种天然存在的具有抗氧化和抗炎活性的多酚。我们研究了迷迭香酸对气管内给予DEP（500微克/只）诱导的小鼠肺损伤的影响。口服补充迷迭香酸（2毫克/只，共3天）可抑制DEP诱导的肺损伤，其特征为中性粒细胞滞留和间质水肿。DEP增强了角质形成细胞趋化因子（KC）、白细胞介素-1β、单核细胞趋化蛋白-1和巨噬细胞炎性蛋白-1α在肺中的表达，而迷迭香酸处理可抑制这种表达。DEP增强了肺中诱导型一氧化氮合酶（iNOS）mRNA的表达以及硝基酪氨酸和8-羟基脱氧鸟苷（8-OHdG）的形成，迷迭香酸也可抑制这些变化。这些结果表明，迷迭香酸通过减少促炎分子的表达来抑制DEP诱导的肺损伤。迷迭香酸的抗氧化活性也可能有助于其保护作用。
