Fuzheng Xuanfei Huashi prescription suppresses inflammation in lipopolysaccharide-induced lung injury in mice toll-like recptor 4/nuclear transcription factor κB and cyclooxygenase-2/prostaglandin E2 pathway.

Objective: To determine the effect of Traditional Chinese Medicine (TCM) Fuzheng Xuanfei Huashi prescription (, FZXF) on lipopolysaccharide (LPS)-induced pneumonia in mice and identify the mechanism of FZXF in the treatment of LPS-induced lung inflammation.

Methods: The pneumonia model was established by intraperitoneal injection of 5 mg/kg LPS in mice. Cytokines were detected by enzyme-linked immune-osorbent assay (ELISA), macrophages in lung tissue were determined by immunofluorescence, and pathway-related data were determined by quantitative real-time polymerase chain reaction (qPCR) and Western blot.

Results: The liver, thymus, and spleen index values and the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) obviously increased in LPS-treated mice. FZXF decreased the white blood cell count and reduced the increase in the lung wet weight/dry weight ratio caused by LPS. The hematoxylin-eosin staining result showed that FZXF could maintain the integrity of lung tissue structure, alleviate interstitial oedema and alveolar wall thickening, and reduce inflammatory cell infiltration. Moreover, FZXF markedly reduced the expression of proinflammatory cytokines. FZXF also significantly reduced LPS-induced malondialdehyde production and increased superoxide dismutase level in the lung. By immunofluorescence, we found that FZXF could reduce macrophage infiltration. The mRNA expression levels of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), toll-like receptor 4 (TLR4) and nuclear transcription factor κB (NF-κB) in the lung tissue of mice were decreased by treatment with FZXF. In addition, FZXF inhibited the protein expression of TLR4, p-p65 and COX-2. These results indicated that FZXF could inhibit the inflammatory response of LPS induced cytokine storm in mice through TLR4/NF-κB and COX-2/PGE2 signaling pathway.

Conclusion: These findings were suggested that FZXF prescription suppresses inflammation in LPS-induced pneumonia in mice via TLR4/NF-κB and COX-2/ PGE2 pathway.