Hepatotoxicity or hepatoprotection of emodin? Two sides of the same coin by < sup > 1 < /sup > H-NMR metabolomics profiling

In this study, 1H NMR based metabolomics approach, complemented with histopathological observation, biochemical measurements, western blotting analysis and real-time quantitative PCR (RT-qPCR), was applied to interpret the paradox of emodin (30 mg/kg, 10 mg/kg BW) using both healthy mice (male, ICR) and chronic CCl4-injured mice (0.1 mL/kg, 0.35% CCl4, 3 times a week for a month). Emodin exerted a weight loss property associated with its lipid-lowing effects, which helped alleviate CCl4-induced steatosis. Emodin effectively ameliorated CCl4-induced oxidative stress and energy metabolism dysfunction in mice liver via regulating glucose, lipid and amino acid metabolism, and inhibited excessive inflammatory response. In healthy mice, emodin only exhibited hepatoxicity on high-dosage by disturbing hepatic anti-oxidant homeostasis, especially GSH and xanthine metabolism. This integrated metabolomics approach identified the bidirectional potential of emodin, which are important for its rational use.PMID:34606778 | DOI:10.1016/j.taap.2021.115734

Source: Toxicology and Applied Pharmacology - October 4, 2021 Category: Toxicology Authors: Lingyu Ruan Lei Jiang Wenlong Zhao Huihui Meng Qi Zheng Junsong Wang Source Type: research