Trigonelline Alleviates <i>Mycoplasma pneumoniae</i> -induced Pneumonia in Mice by Inhibiting ERK/JNK and NF-κB Signaling Pathways

Background Pneumonia continues to represent a significant global health concern, characterized by substantial morbidity and mortality despite advancements in modern medicine. Purpose This respiratory infection remains a leading cause of hospitalization and death worldwide, particularly in developing nations. This study investigated the anti-pneumonia efficacy of trigonelline on Mycoplasma pneumoniae -induced pneumonia in vivo , as well as its underlying mechanisms. Methods BALB/c mice were instilled with 100 µL of M. pneumoniae culture by nasal drops for 3 days. The experimental mice were then treated with 25 mg/kg of trigonelline for 7 days. The Pulmonary Index (PI) and survival index of the experimental mice were assessed. The concentrations of C-reactive protein (CRP), M. pneumoniae -specific IgM, and proinflammatory cytokines were evaluated utilizing the kits. The concentrations of NF-κB, JNK1/2, and ERK1/2 in lung tissues of experimental mice were assessed by utilizing kits. Results The treatment with trigonelline significantly reduced the mortality rate and prolonged the survival rate of the M. pneumoniae -induced mice. Trigonelline treatment also diminished the levels of PI, CRP, M. pneumoniae -specific IgM, and proinflammatory markers in the pneumonia-induced mice. Moreover, trigonelline positively regulated the nuclear factor-κB and extracellular signal-regulated kinase/c-Jun N-terminal kinase signaling in the lung tissues of the M. pneumoniae -induced murine model. Conclusion The present findings demonstrate the therapeutic effectiveness of trigonelline in pneumonia-induced mice. Hence, it can be suggested that trigonelline may serve as a viable therapeutic option for treating pneumonia.