Flavokawain A Mitigates Mycoplasma pneumoniae-Induced Pneumonia by Inhibiting ERK/JNK/NF-κB Pathway in a Mouse Model.

Abstract

Pneumonia, a respiratory infection that primarily affects the lungs, is a significant health concern in the pediatric population, often leading to hospitalization and, in severe cases, mortality. The present study was performed to investigate the therapeutic effects of the flavokawain A against mycoplasma pneumonia in mice. BALB/c mice were subjected to an exposure with 100 µL of Mycoplasma pneumoniae (Mp) via nasal drips for a duration of 2 days, and subsequently administered 50 mg/kg of flavokawain A for a duration of 3 days. The pulmonary index (PI), survival percentage, and survival time was assessed in the experimental mice. The inflammatory biomarker concentrations (MPO and NO), oxidative stress biomarkers (MDA, SOD, and GSH), C-reactive protein (CRP), Mp-specific Ig-M, and inflammatory cytokines were analyzed with the appropriate assay kits. The Mp-DNA concentration were assessed in the experimental mice. The concentrations of JNK, ERK, and NF-κB in the lung tissues were assessed using kits. The histopathological examination was conducted on lung tissues to evaluate the histological alterations. The flavokawain A treatment significantly reduced the lethality and increased survival time in Mp-induced mice. It also diminished the PI, NO, and MPO concentrations in Mp-induced mice. The flavokawain A administration resulted in a reduction of MDA levels and an enhancement of antioxidants SOD and GSH levels. Flavokawain A treatment significantly diminished the levels of inflammatory cytokines, CRP, Mp-specific Ig-M, and Mp-DNA content in the Mp-infected mice. The histological results demonstrated a significant reduction in inflammatory signs and alveolar injury in the Mp-induced mice. The current findings confirm the salutary properties of flavokawain A against Mp-infected mice. Consequently, flavokawain A may serve as a talented therapeutic agent to treat pneumonia.