Effect of Pu-erh tea on acetaminophen-induced hepatotoxicity assessed by physiological, metabolomic, and transcriptomic analyses

Abstract

• PTE pretreatment ameliorated oxidative stress, inflammatory response, and apoptosis of mice caused by excess APAP. • PTE pretreatment and APAP overdose altered the metabolic profile and gene expression of liver tissues. • PTE induced tyrosine and caffeine metabolism, and alleviated hepatotoxicity induced by excess APAP. • Six DEMs and 10 DEGs were biomarkers and key genes for liver protection in high dose APAP exposure. Acetaminophen (APAP) is a painkiller that can cause hepatotoxicity if taken in excess. We investigated the effect of pu-erh tea extract (PTE) on hepatotoxicity induced by excess APAP using physiological, metabolomic, and transcriptomic analyses. PTE decreased levels of oxidative stress, inflammatory response, and apoptosis markers induced by excess APAP. And 156 metabolites and 703 genes were identified as differentially expressed metabolites and differentially expressed genes, respectively. KEGG enrichment analysis revealed that PTE and overdose of APAP altered tyrosine, caffeine, and amino acid-related metabolism. Six differentially expressed metabolites associated with these pathways have hepatoprotective effects and were upregulated by PTE pretreatment. The expression levels of 10 vital differentially expressed genes regulating these metabolites were verified by qRT-PCR. The findings confirm the beneficial role of PTE pretreatment in alleviating the hepatotoxicity caused by overdose of APAP, indicating that PTE can be used as an effective dietary supplement for the development of functional foods.