ArticleCell biochemistry and biophysics2026
Rhein Prevents APAP-induced drug-induced Liver Injury by Upregulating Nrf2 and Inhibiting APAP-activating Enzymes.
Article in Cell biochemistry and biophysics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Severe liver injury can result from an overdose of acetaminophen (APAP). Rhein (RA) has shown a strong capability of combating inflammation and oxidative stress. Our study aimed to investigate the potential of RA in protecting the liver from APAP-induced damage and elucidate the mechanism of action. C57BL/6 mice received a pretreatment with intragastric 100 mg/kg/day RA, followed by 400 mg/kg/day APAP intraperitoneally. Liver injury was assessed via histopathology (hematoxylin and eosin (HE)-staining), serum biochemical indicators. AML-12 cells were treated with APAP or RA, and oxidative stress and apoptosis markers were evaluated. The underlying molecular mechanisms were examined by Western blotting (WB) and quantitative Real-time polymerase chain reaction (qPCR). RA treatment significantly alleviated hepatic injury caused by APAP in rodent model, reduced oxidative stress and apoptosis, and exerted a cytoprotective effect on AML-12 cells. RA increased intracellular glutathione (GSH) content and the GSH/GSSG (Glutathione disulfide) ratio, thereby enhancing the GSH redox cycle through the Nrf2 (Nuclear factor erythroid 2–related factor 2)-GCL (glutamate cysteine ligase)/GSR (glutathione-disulfide reductase) pathway. In addition, RA inhibited the expression of CYP2E1 and CYP1A2, the enzymes converting APAP into the NAPQI (N-acetyl-p-benzoquinone imine), thus effectively mitigating APAP-induced DILI (Drug Induced Liver Injury). We identified that RA prevents APAP-induced DILI liver injury by upregulating Nrf2 and inhibiting APAP-activating enzymes.
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