Qiangli Wuhu mixture alleviates LPS-induced pneumonia by inhibiting the TLR4/NF-κB/NLRP3 pathway: a study based on network pharmacology

Background: This study aimed to clarify the mechanism of action of Qiangli Wuhu Mixture used in the treatment of pneumonia.Methods: The potential targets of Qiangli Wuhu Mixture in the treatment of pneumonia were predicted by network pharmacology. ICR male mice were randomly divided into 5 groups: normal control (Control), pneumonia model (Vehicle), low and high dose groups of Qiangli Wuhu Mixture, and dexamethasone positive control group with 12 mice in each. The model was established by tracheal instillation of lipopolysaccharide for 3 consecutive days. After the establishment of the animal model, Qiangli Wuhu Mixture was intragastrically administered for 5 days; the expression of inflammatory factors tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and anti-inflammatory factor interleukin-10 (IL-10) in the serum of mice in each group was detected by ELISA kit; the protective effect of Qiangli Wuhu Mixture on the lung tissue of pneumonia mice was observed by staining; Western Blot was used to detect the expression of Toll-like receptor 4 (TLR4), nuclear factor kappa B (NF-κB) and NLRP3 signal pathway related proteins in lung tissue.Results: Network pharmacology predicted that the target of Qiangli Wuhu Mixture in treating pneumonia might be related to lipopolysaccharide reaction and Toll-like receptor signaling pathway. the in vivo results indicated that Qiangli Wuhu Mixture had a strong protective effect on acute pneumonia in mice induced by lipopolysaccharide, decreased the levels of inflammatory factors TNF-α, IL-1β and IL-6 in serum of model mice, and decreased the activation of TLR4, NF- κ B, and the expression of NLRP3 protein in lung tissue. Conclusion: Qiangli Wuhu Mixture has a strong protective effect on lipopolysaccharide-induced pneumonia in mice, and its mechanism of action may be related to reducing the pathological changes of lung tissue, reducing the level of inflammatory cytokines in blood, and inhibiting the inflammatory signal pathway of TLR4/NF-κB/NLRP3.