Biomedicine & Pharmacotherapy (Apr 2020)

GC-MS based metabolomic profiling of lung tissue couple with network pharmacology revealed the possible protection mechanism of Pudilan Xiaoyan Oral Liquid in LPS-induced lung injury of mice

  • Gang Tian,
  • Chao Li,
  • Yuanyuan Zhai,
  • Jia Xu,
  • Li Feng,
  • Weifeng Yao,
  • Beihua Bao,
  • Li Zhang,
  • Anwei Ding

Journal volume & issue
Vol. 124
p. 109833

Abstract

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Pudilan Xiaoyan Oral Liquid (PDL) originated from ''Pudilan'' Classic Recipe of traditional Chinese medicine is one kind of anti-inflammatory Chinese patent medicine recorded in Chinese Pharmacopeia. PDL has been used clinically for treating inflammatory diseases of the respiratory tract. However, due to the complex composition of PDL, its potential anti-inflammation and the mechanism remain unknown. To identify the mechanism of the PDL in the treatment of lipopolysaccharide (LPS)-induced lung injury of mice. The mice models of lung injury were established and the changes of biochemical indices in serum and histopathology were detected to explore the effects of PDL. The approach of GC–MS metabolomics was used to find more significant metabolites, and the metabolic pathways were enriched through MetaboAnalyst. Then network analysis was applied to visualize the protein related to the important metabolites, merging into a protein-metabolite network via Cytoscape. The treatment of PDL could attenuate LPS-induced histopathological damage of lung tissues, followed by reducing pro-inflammation mediators including IL-10, TNF-a and NF-ĸB in serum. 11 potential metabolites were identified in lung tissue through metabolomics, which were significantly regulated to recover by PDL treatment. The correlated network was constructed by integrating potential metabolites and pathways. Aspartate and l-cysteine were selected as key metabolites and correlated proteins such as IL4I1 and ASPA were speculated as the potential target to treat LPS-induced lung injury using PDL. These results demonstrated that PDL might prevent the pathological process of lung injury through regulating the disturbed protein-metabolite network.

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