Physalin A alleviates inflammation and oxidative stress in mouse infantile pneumonia by inhibiting JAK/STAT3 and NF κB pathways

Abstract

Purpose: To investigate the effect of physalin A on infantile pneumonia in mice.
 Methods: A mouse model of infantile pneumonia was established via intraperitoneal injection of lipopolysaccharide and verified using hematoxylin and eosin staining. Lipopolysaccharide-stimulated mice were then administered physalin A. The total protein content, number of cells, and levels of inflammatory-factor in bronchoalveolar lavage fluid (BALF) were determined. Inflammation and oxidative stress levels in lung tissues were determined by enzyme-linked immunosorbent assay (ELISA).
 Results: Lipopolysaccharide injection induced shrinking of pulmonary alveoli in mice, but physalin A administration ameliorated the histopathologic damage in lung tissues and significantly reduced the total protein content and number of cells in the BALF of lipopolysaccharide-stimulated mice (p < 0.001). Moreover, physalin A also significantly down-regulated the levels of tumor necrosis factor-α, interleukin (IL)-6, IL-18, and IL-1β in BALF and lung tissues of lipopolysaccharide-treated mice (p < 0.001). Physalin A attenuated lipopolysaccharide-induced increases in malondialdehyde and myeloperoxidase as well as decreases in superoxide dismutase and glutathione in mouse lung tissues. Additionally, physalin A reduced the levels of p-JAK1, p-STAT3, and p-p65 in lung tissues of lipopolysaccharide-treated mice.
 Conclusion: Physalin A exerts anti-inflammatory and anti-oxidant effect on lipopolysaccharide-induced lung injury in mice through the inactivation of JAK/STAT3 and NF-κB pathways. However, the effect of Physalin A on inflammation and oxidative stress in lipopolysaccharide-induced A549 cells will need to be investigated in further studies.