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Background. This study discusses the anti-inflammatory mechanism of Yiqi Huayu Jiedu decoction (YQHYJD) and studies the intervening effect of YQHYJD on the inflammatory cytokines in acute respiratory distress syndrome (ARDS) rats by inhibiting the TLR4/NLRP3 signal pathway. The aim of the probe is to provide evidence to support the identification of therapeutic targets in Chinese medicine treatment, which broadens the alternatives for the treatment of ARDS. Method. A lipopolysaccharide (LPS)-induced ARDS model group is established on rats by tail vein injection. A medicine group is established on ARDS rats by prophylactic administration using YQHYJD. Materials are collected, and tests are conducted according to experimental processes. Result. The rats in the medicine group gained weight compared with those in the ARDS model group. Pathological sections from the medicine group indicated improved condition in terms of pulmonary and interstitial edema in the lung tissues of rats compared with that from the ARDS model group. The percentage of neutrophil of the medicine group was significantly brought down compared with that of the ARDS model group (P < 0.001). Enzyme-linked immunosorbent assay (ELISA) was used to detect the changes in the level of inflammatory cytokines. It was observed that the levels of IL-1β and IL-18 in serum of the medicine group significantly decreased (P < 0.001 and P < 0.01), the contents of TLR4 and NLRP3 in bronchoalveolar lavage fluid (BALF) of the medicine group decreased, and the contents of TLR4 and NLRP3 in lung tissue homogenate of the medicine group significantly decreased (P < 0.05 , P < 0.001 , P < 0.01 , and P < 0.05). In further mass spectrum identification of the proteins from the same animal groups, it was observed that the expressions of inflammatory proteins TNFRSF1, LBP, and NOS2 of the medicine group were reduced. The differences were statistically significant. Conclusions. The pharmacological action of YQHYJD's anti-inflammatory mechanism is closely associated with the regulation of inflammatory cytokines TLR4, NLRP3, IL-1β, IL-18, TNFRSF1, LBP, and NOS2 on the TLR4/NLRP3 signal pathway. [ABSTRACT FROM AUTHOR]

Special electromagnetic field-treated water (SEW) and far-infrared radiation (FIR) can reduce acute respiratory distress syndrome (ARDS) in rats inflicted by lipopolysaccharides (LPSs). However, little is known about its underlying molecular mechanism. Differentially expressed proteins (DEPs) of SEW and FIR interventions were obtained from a proteomics database. A total of 89 DEPs were identified. Enrichment analysis of DEPs was performed using the Database for Annotation, Visualization, and Integrated Discovery. These DEPs were associated with the responses to LPSs, acute inflammation, extracellular exosomes, glucocorticoids, and electrical stimuli. The protein-protein interaction network was set up using the STRING database. Modular analysis was performed using MCODE in the Cytoscape software. Proteins Haptoglobin, Apolipoprotein B, Transthyretin, and Fatty acid binding protein 1 were among the core networks. A tail vein injection of LPS was used to establish the rat model with ARDS. Parallel reaction monitoring confirmed Hp protein expression. Inflammatory pathway factors were detected using an enzyme-linked immunosorbent assay. This indicates that SEW and FIR can be considered as potential clinical treatment methods for ARDS treatment and that their functional mechanisms are related to the ability of alleviating lung inflammation through Hp protein adjustment.