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

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.

Automated summary

This study investigated the effect of pu-erh tea extract (PTE) on hepatotoxicity induced by excess acetaminophen (APAP). Results showed that PTE reduced oxidative stress, inflammatory response, and apoptosis induced by excess APAP. Metabolomic and transcriptomic analyses identified differentially expressed metabolites and genes related to tyrosine, caffeine, and amino acid metabolism.