Aurantiamide Acetate Ameliorates Lung Inflammation in Lipopolysaccharide‐Induced Acute Lung Injury in Mice
Zhengyu Fang, Jie Fang, Chunxiao Gao, Yueguo Wu, Wen-Ying Yu
Abstract
Purpose . Aurantiamide acetate (AA) is a dipeptide derivative with complex pharmacological activities and remarkable effects on preventing and treating various diseases. In the current study, we aimed to investigate whether AA can exert protective effects in a mouse model of ALI induced by LPS. Materials and Methods . In this model, mice were given intranasal LPS for 3 days prior to receiving AA (2.5, 5, and 10 mg/kg) via oral gavage. An assessment of histopathological changes was performed by hematoxylin and eosin (HE). Proinflammatory cytokines were detected in bronchoalveolar lavage fluids (BALFs) by enzyme‐linked immunosorbent assays (ELISAs). The effects of AA on protein expression of NF‐ κ B and PI3K/AKT signaling pathways were determined by Western blot. In addition, lung wet/dry (W/D) weight ratio, myeloperoxidase (MPO) activity, cell counts, and protein content were also measured. Results . According to results, AA pretreatment significantly reduced lung pathological changes, W/D ratio, MPO activity, and protein content. Additionally, AA resulted in a significant reduction in the number of total cells, neutrophils, and proinflammatory cytokines in the BALF after LPS stimulation. The subsequent study revealed that pretreatment with AA dose dependently suppressed LPS‐induced activation of NF‐ κ B as well as PI3K/AKT phosphorylation. Conclusion . The results indicated that the AA had a protective effect on LPS‐induced ALI in mice and could be a potential drug for ALI.