Mechanism of ligustrazine in alleviating biliary atresia-associated liver fibrosis by regulating the TGF-β/Smad pathway and inhibiting hepatocyte pyroptosis

April 1, 2026Lishizhen medicine and materia medica research

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This research investigates the role of ligustrazine in alleviating liver fibrosis linked to biliary atresia by modulating the TGF-beta/Smad pathway and inhibiting hepatocyte pyroptosis.
Conducted animal experiments with C57BL/6 mice divided into treatment groups over 14 days.
Performed histological assessments and biochemical analyses including serum AST, ALT, and Western blot for various proteins associated with fibrosis and inflammation.
Developed an in vitro model with HSC-T6 cells treated with TGF-beta1, followed by ligustrazine administration to assess cellular changes and signal pathways.
The model group exhibited significant liver fibrosis, cell necrosis, and increased collagen deposition, along with elevated AST and ALT levels (P<0.001).
Key proteins related to pyroptosis and inflammation, such as ASC and NLRP3, showed a marked increase (P<0.001; P<0.0001), while TGF-beta signaling proteins displayed significant alterations after treatment.
Ligustrazine treatment effectively reversed fibrosis and corrected the dysregulated TGF-beta/Smad pathway, with consistent results in both animal and cellular models.

Animal experiments demonstrate ligustrazine's effectiveness in reducing liver fibrosis in biliary atresia, suggesting a new therapeutic approach.

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MENG et al. (2026) studied this question.

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