栀子苷对小鼠急性肺损伤保护机制的研究

为了探究栀子苷能否对脂多糖(LPS)致小鼠急性肺损伤发挥保护作用及其潜在的作用机制。雄性Balb/c小鼠，于鼻腔滴注LPS前1 h腹腔注射栀子苷(50 mg/kg)或者地塞米松注射液(5 mg/kg)，滴注LPS 24 h后，采用酶联免疫吸附法(ELISA)测定小鼠支气管肺泡灌洗液(BALF)中肿瘤坏死因子-α(TNF-α)、白介素(IL)-6和IL-10的浓度。通过细胞分类计数法分析BALF中细胞总数、巨噬细胞和中性粒细胞的变化。采用蛋白印迹法(Western-blot)分析核转录因子-κB（NF-κB）信号转导通路激活的程度。腹腔注射栀子苷可降低小鼠肺干湿比（W/D值）；改善肺组织病理学结构，减少肺泡出血和炎性细胞浸润且伴有髓过氧化物酶活性下降；抑制促炎性细胞因子TNF-α和IL-6分泌，促进抗炎性细胞因子IL-10生成。栀子苷通过缓减炎症反应保护LPS致小鼠急性肺损伤，其机制可能与阻止NF-κB信号转导通路的激活有关。

Geniposide Protects against Lipopolysaccharide-induced Acute Lung Injury in Mice

The purpose of this study was to evaluate the effect of geniposide on acute lung injury （ALI） induced by lipopolysaceharide （LPS） in mice. Male BALB/e mice were pretreated with dexamethasone （DEX） or geniposide 1 h before intranasal instillation of LPS. Seven hours after LPS challenge, the levels of tumor necrosis faetor-α （TNF-α）, interleukin-6 （IL-6）, and interleukin-10 （IL-10） in the bronchoalveolar lavage fluid （BALF） were measured. The number of total cells, neutrophils, and maerophages in the BALF were also determined. The extent of IκB phosphorylation was detected by Western-blot. Pretreatment with geniposide was found to decrease the W/D ratio of the lung tissue; attenuate lung histopathologic changes, alveolar hemorrhage, and neutrophil infiltration, with evidence of reduced myeloperoxidase （MPO） activity; down-regulate the level of pro-inflammatory mediators, including TNF-α and IL-6; up-regulate the concentration of IL-10; and inhibit the phosphorylation of IκB. Taken together, our results suggested that Geniposide might provide protective effects against LPS-induced ALI by mitigating the inflammatory response and that the compound＇ s mechanism of action might involved blocking the nuclear faetor-kappaB （NF-κB） signaling pathway activation.