Pediatric pneumonia is a common respiratory disease and Yinlai Decoction (YLD) is a commonly used treatment in China. We explored the anti-inflammatory mechanism of action of this traditional Chinese medicine for pneumonia.

We studied, by experimentation, the mechanism of action of YLD in treating pneumonia according to network pharmacology. By comparing YLD with dexamethasone (DXMS), we investigated the efficacy of YLD in treating pneumonia induced by lipopolysaccharide (LPS) in juvenile rats.

In an aqueous extract of YLD, 22 chemical compounds were identified, among which 10 were related to inflammation, involving 78 target genes and 16 signaling pathways. Among them, 45 core target proteins were related to biologic processes and functions, such as response to stimuli, biologic regulation, cell communication and protein binding. Animal experiments showed that YLD relieved pulmonary inflammation and demonstrated no significant damage to the liver, spleen or kidneys of rats. YLD could regulate expression of inflammatory cytokines in serum and inflammation-related proteins in lung tissues to some extent, but its effect is less significant than that of DXMS.

YLD protected juvenile rats against LPS-induced pneumonia, and showed fewer side effects in comparison with DXMS. YLD could be efficacious treatment for pediatric respiratory infections and even pneumonia.

To examine the effects of accumulated heat in GI tract (AHGIT) on lung tissue protein expression in pneumonic mice.

Nebulized lipopolysaccharides (LPS) were administered to induce a pneumonic mouse model (M1), and a high-calorie/protein diet combined with nebulized LPS was used to induce AHGIT pneumonia (M2). Isobaric tag for relative and absolute quantitation (iTRAQ) proteomics was applied to study lung protein expression, followed by bioinformatics analysis.

M1 mice developed alveolar damage with prominent septum thickening, vascular dilation, hyperaemia and infiltration of large amounts of inflammatory cells. M2 mice developed more severe pathological responses. A total of 2626 proteins were reliably identified in the lung tissue. Compared with normal mice, the M1 mice had 344 differentially expressed proteins in their lungs, which are involved in the following biological processes: response to organic substance, response to cytokine, response to external stimulus, defense response and immune system process. They are also involved in the following Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways: ECM-receptor interaction, leukocyte transendothelial migration, Fc gamma R-mediated phagocytosis, complement and coagulation cascades, and antigen processing and presentation. Compared with the M1 group, the M2 mice had 164 differentially expressed proteins in their lungs, including 14 upregulated and 150 downregulated proteins. These proteins are involved in the following biological processes: small molecule metabolism, ribose phosphate metabolic process, cell adhesion and biological adhesion. The relevant KEGG pathways included oxidative phosphorylation, Citrate cycle (TCA cycle), complement and coagulation cascades, and vascular smooth muscle contraction.

AHGIT aggravated the lung inflammatory damage in the mice with LPS-induced pneumonia. It may affect the mouse substance/energy metabolism, and therefore the immune function, to aggravate the LPS-induced inflammatory damage.