Protective effect of Ganoderma atrum polysaccharides in acute lung injury rats and its metabolomics

• Published in: International journal of biological macromolecules Vol. 142; pp. 693 - 704
• Main Authors: Li, Lu, Fu, Wang-wei, Wu, Rui-ting, Song, Ye-hao, Wu, Wen-ying, Yin, Shu-hua, Li, Wen-juan, Xie, Ming-yong
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.01.2020
• Subjects: Acute lung injury; Gnaoderma atrum polysaccharide; Inflammation; Metabolism; AA; Acute lung injury; NO; IL; PSG; H&E; OPLS-DA; Inflammation; Metabolism; LPS; PCA; Gnaoderma atrum polysaccharide; TNF-α; IDO; DEX; WBC; GC; VIP; ALI; TDO
• ISSN: 0141-8130; 1879-0003
• DOI: 10.1016/j.ijbiomac.2019.10.010

[Display omitted] •PSG exhibited benefical effects by inhibiting metabolism disturbances.•Several metabolism pathways were notably modified by PSG treatment in ALI rats.•PSG could improve gut microbial metabolite short-chain fatty acids in ALI rats.•PSG displayed anti-inflammatory effects in LPS-induced acute lung injury (ALI) rats. The present study aimed to evaluate effect of Ganoderma atrum polysaccharide (PSG) on acute lung injury (ALI) rats and its mechanisms. Results showed that PSG exhibited protective effects against ALI by maintaining pulmonary histology, reducing levels of pro-inflammatory cytokines and NO both in serum and lung tissue. Moreover, this study further evaluated the metabolic effects of PSG based on UPLC-Triple-TOF/MS metabolomics analysis in rats. Compared with control group, LysoPC (18:2), LPA (18:1), taurocholic acid, L-histidine, and L-tryptophan were identified as metabolic biomarkers in serum of ALI group. Furthermore, biological pathways analysis demonstrated that histidine metabolism, nitrogen metabolism, tryptophan and part glycerophospholipids metabolism were notably modified by PSG treatment in ALI rats. Additionally, improved gut microbial metabolite short-chain fatty acids were found after intake of PSG in ALI rat. Altogether, PSG could control ALI-induced aberrant inflammation and its mechanisms were linked to inhibit release of pro-inflammatory mediators and reverse metabolic pathway disturbances.