Abstract
An integrated method combining network pharmacology and in vivo experiment was performed to investigate the therapeutic mechanism of capsaicin (Cap) against acute lung injury. The potential key genes and signaling pathways involved in the therapeutic effect of Cap were predicted by the network pharmacology analyses. Additionally, the histological assessment, ELISA, and RT-qPCR were performed to confirm the therapeutic effect and the potential mechanism action involved. Our findings showed that TNF, IL-6, CXCL1, CXCL2, and CXCL10 were part of the top 50 genes. Enrichment analysis revealed that those potential genes were enriched in the TNF signaling pathway and IL-17 signaling pathway. In vivo experiment results showed that Cap alleviated histopathological changes, decreased inflammatory infiltrated cells and inflammatory cytokines, and improved antioxidative enzyme activities in the bronchoalveolar lavage fluid (BALF). Furthermore, Cap treatment effectively downregulated TNF, IL-6, NF-κB, CXCL1, CXCL2, and CXCL10 in lung tissue. Thus, our findings demonstrated that Cap has the therapeutic effect on LPS-induced acute lung injury in neonatal rats via suppression of the TNF signaling pathway and IL-17 signaling pathway.
Highlights
Acute lung injury is the initial stage of the entire pathological progression of acute respiratory distress syndrome
Based on SwissTargetPrediction and CTD databases, 621 potential genes of Cap were collected after the deletion of duplicate genes
621 potential genes from Cap were combined with 28,815 acute lung injury-related genes by using a Venn tool to identify the potential genes of Cap against acute lung injury
Summary
Acute lung injury is the initial stage of the entire pathological progression of acute respiratory distress syndrome. It is a life-threatening inflammatory syndrome with high mortality and morbidity [1]. Acute respiratory distress syndrome is the more severe manifestation of acute lung injury, which is characterized by lung inflammation, pulmonary edema, diffuse alveolar damage, and increased neutrophil infiltration [2, 3]. It has been reported that uncontrolled pulmonary inflammation is involved in the pathological process of acute lung injury in infants [6]. Current treatment strategies have not been effective in decreasing the mortality and incidence of acute lung injury [7]. It is extremely urgent to develop an effective drug for the treatment of acute lung injury
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