关键词: 抗氧化酶, 抗氧化酶

Abstract:

The purpose of this study was to evaluate the effect of Geniposide on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in mice. Male BALB/c 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 factor-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 macrophages 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 histopathologicchanges, 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 involve blocking the nuclear factor-kappaB (NF-κB) signaling pathway activation.