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May 18, 2026Biomedical Chromatography0 citations

Sophora tonkinensis Alleviates Progression of Diethylnitrosamine‐Induced Hepatocellular Carcinoma in Rats via Multitarget Regulation

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ZLZongliang LuJWJincai WenCLChengwei Li

Key Points

  • The study aims to investigate the effects of Sophora tonkinensis on hepatocellular carcinoma progression in a rat model.
  • Established hepatocellular carcinoma model using diethylnitrosamine in SD rats.
  • Administered Sophora tonkinensis extract orally from Weeks 1 to 16.
  • Conducted transcriptomic and metabolomic analyses alongside quantitative real-time polymerase chain reaction for validation.
  • Sophora tonkinensis extract significantly reduced HCC incidence.
  • Notable weight recovery and decreased liver nodule volume were observed.
  • Improved liver function was indicated by reduced ALT, AST, ALP, and ALB levels.

Abstract

Sophora tonkinensis, a traditional Chinese medicine with heat-clearing, detoxifying, and throat-soothing properties, has shown potential in treating hepatitis, inhibiting tumors, and regulating immunity, but its active constituents and mechanisms remain unclear. We established a hepatocellular carcinoma (HCC) model in SD rats using diethylnitrosamine (DEN), with oral gavage of S. tonkinensis extract (STE) from Weeks 1 to 16, alongside model and normal control groups. Results showed that STE significantly reduced HCC incidence, reversed weight loss, decreased the number and volume of liver nodules, improved histopathological damage, and lowered serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and albumin (ALB) levels. Integrated transcriptomic (RNA-seq) and metabolomic (LC-MS/MS) analyses revealed enrichment in arachidonic acid and glycerophospholipid metabolism. Quantitative real-time polymerase chain reaction (qPCR) validation confirmed that STE restored hepatic lipid homeostasis and alleviated inflammation by activating the peroxisome proliferator-activated receptor (PPAR) pathway and suppressing the IL-17/TGF-β axis. These findings clarify the core mechanisms of STE in preventing and treating HCC, providing a theoretical basis for its precise clinical application.

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Cite This Study

Lu et al. (2026) studied this question.

synapsesocial.com/papers/6a0aacb35ba8ef6d83b7003ehttps://doi.org/10.1002/bmc.70486
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