DOI: 10.57760/sciencedb.27324
title: Original data of "Integrative Metabolomics and Transcriptomics Analysis Reveals Hepatotoxic Mechanisms and Key Toxic Components of Polygoni Multiflori Radix and Polygoni Multiflori Radix Praeparata"
title: Original data of "Integrative Metabolomics and Transcriptomics Analysis Reveals Hepatotoxic Mechanisms and Key Toxic Components of Polygoni Multiflori Radix and Polygoni Multiflori Radix Praeparata"

description: Polygoni Multiflori Radix (PMR) and its processed form, Polygoni Multiflori Radix Praeparata (PMRP), are two widely used traditional Chinese medicines (TCM). Nevertheless, in recent years, frequent reports have emerged regarding their hepatotoxicity. Despite numerous studies, the underlying mechanisms of their hepatotoxicity and the key toxic components remain poorly understood. This work aims to comprehensively clarify the processes of liver damage induced by PMR and PMRP and to identify the principal toxic components. In vivo toxicity tests confirmed that PMR and PMRP can induce cholestatic liver injury. The integration of untargeted serum metabolomics, liver transcriptomics, and liver spatial metabolomics revealed that tryptophan metabolism, the tricarboxylic acid (TCA) cycle, purine metabolism, and glutathione metabolism were primarily regulated, resulting in liver injury. Further mechanism analysis showed that PMR and PMRP can also inhibit the expression of bile acid transporter, causing the obstruction of bile acid secretion. These modulations trigger oxidative stress, subsequently leading to cholestasis. The accumulation of bile acids further intensifies oxidative stress, forming a vicious cycle. Additionally, emodin was identified as the main toxic component. The difference in emodin content in the liver after administration of PMR and PMRP explains the observation that PMR exhibits higher hepatotoxicity.
description: Polygoni Multiflori Radix (PMR) and its processed form, Polygoni Multiflori Radix Praeparata (PMRP), are two widely used traditional Chinese medicines (TCM). Nevertheless, in recent years, frequent reports have emerged regarding their hepatotoxicity. Despite numerous studies, the underlying mechanisms of their hepatotoxicity and the key toxic components remain poorly understood. This work aims to comprehensively clarify the processes of liver damage induced by PMR and PMRP and to identify the principal toxic components. In vivo toxicity tests confirmed that PMR and PMRP can induce cholestatic liver injury. The integration of untargeted serum metabolomics, liver transcriptomics, and liver spatial metabolomics revealed that tryptophan metabolism, the tricarboxylic acid (TCA) cycle, purine metabolism, and glutathione metabolism were primarily regulated, resulting in liver injury. Further mechanism analysis showed that PMR and PMRP can also inhibit the expression of bile acid transporter, causing the obstruction of bile acid secretion. These modulations trigger oxidative stress, subsequently leading to cholestasis. The accumulation of bile acids further intensifies oxidative stress, forming a vicious cycle. Additionally, emodin was identified as the main toxic component. The difference in emodin content in the liver after administration of PMR and PMRP explains the observation that PMR exhibits higher hepatotoxicity.