Forsythoside A inhibited inflammatory response by inhibiting p38 JNK/MAPK/ERK and NF-κB signaling in Staphylococcus aureus pneumonia.

BACKGROUND

S. aureus pneumonia, one of the most common S. aureus-induced diseases, is characterized by infectious inflammation in alveoli, distal airway, and lung interstitial. Forsythiaside A possesses anti-inflammatory, anti-infective, and other pharmacological properties in several diseases. The role of forsythiaside A remains unclear in S. aureus pneumonia.

AIM OF THE STUDY

We aimed to figure out the role of forsythiaside A in S. aureus pneumonia.

METHODS

RAW264.7 cells and C57BL6 mice were infected with S. aureus to construct S. aureus pneumonia cell model and animal model, respectively. A series of experiments including MTT, ELISA, Western blot, H&E staining and EBD staining were operated to figure out the role of forsythiaside A in S. aureus pneumonia.

RESULTS

In RAW264.7 cells, forsythiaside A did not induce cell toxicity but triggered cytokines (TNF-α, IL-6 and IL-1β) release in a dose-dependent manner. Moreover, forsythiaside A inhibited p38 JNK/MAPK/ERK and NF-κB pathways by repressing phosphorylation of p38, JNK, ERK and p65 proteins. For in vivo study, forsythiaside A improved survival rate of S. aureus pneumonia mice by alleviating lung injury. In addition, forsythiaside A protected from air-blood barrier destruction and pulmonary edema. At last, forsythiaside A inhibited neutrophils infiltration and inflammatory response in bronchoalveolar lavage fluid.

CONCLUSIONS

Forsythoside A inhibited inflammatory response by inhibiting p38 JNK/MAPK/ERK and NF-κB signaling in S. aureus pneumonia, which provided a novel insight for S. aureus pneumonia treatment.