Graduate Institute of Chinese Medical Science, China Medical University, Taichung 404, Taiwan.
Evid Based Complement Alternat Med. 2013;2013:976342. doi: 10.1155/2013/976342. Epub 2013 Aug 13.
Traditional Chinese medicine formula Sheng-Fei-Yu-Chuan-Tang (SFYCT), consisting of 13 medicinal plants, was used to treat patients with lung diseases. This study investigated the immunoregulatory effect of SFYCT on intratracheal lipopolysaccharides- (LPS-) challenged acute lung injury (ALI) mice. SFYCT attenuated pulmonary edema, macrophages, and neutrophils infiltration in the airways. SFYCT decreased inflammatory cytokines, including tumor necrosis factor- α (TNF α ), interleukin-1 β , and interleukin-6 and inhibited nitric oxide (NO) production but increased anti-inflammatory cytokines, interleukin-4, and interleukin-10, in the bronchoalveolar lavage fluid of LPS-challenged mice. TNF α and monocyte chemotactic protein-1 mRNA expression in the lung of LPS-challenged mice as well as LPS-stimulated lung epithelial cell and macrophage were decreased by SFYCT treatment. SFYCT treatment also decreased the inducible nitric oxide synthase expression and phosphorylation of nuclear factor- κ B (NF- κ B) in the lung of mice and macrophage with LPS stimulation. SFYCT treatment dose dependently decreased the LPS-induced NO and reactive oxygen species generation in LPS-stimulated macrophage. In conclusion, SFYCT attenuated lung inflammation during LPS-induced ALI through decreasing inflammatory cytokines production while increasing anti-inflammatory cytokines production. The immunoregulatory effect of SFYCT is related to inhibiting NF- κ B phosphorylation.
中药方剂生脉愈喘汤（SFYCT）由 13 种药用植物组成，用于治疗肺部疾病患者。本研究探讨了 SFYCT 对气管内脂多糖（LPS）诱导的急性肺损伤（ALI）小鼠的免疫调节作用。SFYCT 减轻了 LPS 诱导的 ALI 小鼠的肺水肿、巨噬细胞和中性粒细胞气道浸润。SFYCT 降低了炎症细胞因子，包括肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6，并抑制了一氧化氮（NO）的产生，但增加了抗炎细胞因子白细胞介素-4（IL-4）和白细胞介素-10，在 LPS 刺激的小鼠支气管肺泡灌洗液中。SFYCT 处理还降低了 LPS 刺激的肺上皮细胞和巨噬细胞中 TNF-α和单核细胞趋化蛋白-1mRNA 的表达。SFYCT 处理还降低了 LPS 诱导的肺中诱导型一氧化氮合酶表达和核因子-κB（NF-κB）的磷酸化在 LPS 刺激的巨噬细胞中。SFYCT 处理剂量依赖性地降低了 LPS 诱导的 NO 和 LPS 刺激的巨噬细胞中活性氧的产生。总之，SFYCT 通过减少炎症细胞因子的产生，同时增加抗炎细胞因子的产生，减轻了 LPS 诱导的 ALI 期间的肺部炎症。SFYCT 的免疫调节作用与抑制 NF-κB 磷酸化有关。
