Preventive Effect and Mechanism of Ganoderma lingzhi Polysaccharides on Acute Alcoholic Liver Injury in Mice

To explore the preventive effect and mechanism of Ganoderma lingzhi polysaccharides on acute alcoholic liver injury in mice.

G. lingzhi polysaccharides were extracted by hot water extraction and identified by Fourier transform infrared spectroscopy (FTIR). Mice were randomly divided into five groups: blank, model, G. lingzhi mycelial polysaccharides (GLMPS) (200 mg of GLMPS/kg m_b), G. lingzhi fruiting body polysaccharides (GLFPS) (200 mg of GLFPS/kg m_b), and positive control (300 mg of biphenyl diester/kg m_b). Sobering-up and drunkenness time, liver index and the levels of malondialdehyde (MDA), catalase (CAT) and superoxide dismutase (SOD) were measured in all groups. RNA was extracted from the liver tissue of experimental mice for transcriptomic analysis of the action mechanism of G. lingzhi polysaccharides and its verification by real-time fluorescence quantitative polymerase chain reaction (qPCR).

Both G. lingzhi polysaccharides prolonged the drunkenness time of mice with alcoholic liver injury, shortened the sobering-up time, decreased the liver index, inhibited the increase in MDA, increased the levels of CAT and SOD, and significantly improved cellular swelling and foam-like changes, GLFPS being more effective than GLMPS. Totally 94 differentially expressed genes (DEGs) were identified. Gene ontology (GO) analysis showed that these DEGs were mainly related to the metabolic processes of fatty acids and monocarboxylic acid, insulin-like growth factor, and glutathione transferase activity. Kyoto encyclopedia of genes and genomes (KEGG) enrichment results showed that the main pathways involving DEGs were glutathione metabolism, cytochrome P450, and retinol metabolism. The real-time fluorescence qPCR results showed that the up-regulation or down-regulation of genes in response to alcohol was alleviated in the GLFPS group, proving the accuracy of transcriptomic analysis.

G. lingzhi polysaccharides effectively prevent acute alcoholic liver injury, and its mechanism may be related to regulation of the expression of the genes associated with glutathione metabolism, cytochrome P450, and retinol metabolism.