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<p>Aflatoxin B1 (AFB1) is a potent hepatotoxin that induces oxidative stress, inflammation, and mitochondrial dysfunction. Dipsacoside B (DB), a bioactive triterpenoid saponin from <i>Flos Lonicerae</i> (Shanyinhua), is recognized for its antioxidant, anti-inflammatory, and cytoprotective properties. This study investigates the protective effects of DB against AFB1-induced liver injury and the underlying mechanisms. Male C57BL/6 mice were assigned to control, AFB1, DB, and AFB1 + DB groups, receiving oral treatments for 4 weeks. The results showed that DB significantly alleviated AFB1-induced weight loss and liver damage, as evidenced by histopathological changes and serum biochemical markers. DB reduced hepatic H₂O₂ and MDA levels, enhanced the activities of antioxidant enzymes such as T-SOD, GSH-Px, CAT, and total antioxidant capacity (T-AOC), inhibited the expression of IL-6, IL-1β, and TNF-α genes, and modulated metabolic enzymes by downregulating Phase I genes (CYP1A2, CYP3A11) while upregulating the Phase II gene GSTA3. Notably, DB upregulated AFB1-suppressed Nrf2 and its downstream targets (HO-1, NQO1, SOD1, GCLC, GCLM, GSS). DB also reversed AFB1-induced mitochondrial damage, including swelling and cristae disruption, and inhibited apoptosis by restoring Bcl-2 and reducing p53, Bax, Cyt-c, caspase-9, and caspase-3 expression. These findings suggest that DB protects against AFB1-induced liver injury by regulating oxidative stress, inflammation, apoptosis, and metabolic enzymes, suggesting it has significant potential as a therapeutic strategy for aflatoxin-related hepatic disorders.</p>

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Dipsacoside B alleviates aflatoxin B1-induced liver injury in mice

  • 期刊论文

  • 发表日期：

    2026年2月21日

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  • Sicong Li,
  • Min Zhang,
  • Bin Wang,
  • Ge Liang,
  • Xuting Li

摘要

Aflatoxin B1 (AFB1) is a potent hepatotoxin that induces oxidative stress, inflammation, and mitochondrial dysfunction. Dipsacoside B (DB), a bioactive triterpenoid saponin from Flos Lonicerae (Shanyinhua), is recognized for its antioxidant, anti-inflammatory, and cytoprotective properties. This study investigates the protective effects of DB against AFB1-induced liver injury and the underlying mechanisms. Male C57BL/6 mice were assigned to control, AFB1, DB, and AFB1 + DB groups, receiving oral treatments for 4 weeks. The results showed that DB significantly alleviated AFB1-induced weight loss and liver damage, as evidenced by histopathological changes and serum biochemical markers. DB reduced hepatic H₂O₂ and MDA levels, enhanced the activities of antioxidant enzymes such as T-SOD, GSH-Px, CAT, and total antioxidant capacity (T-AOC), inhibited the expression of IL-6, IL-1β, and TNF-α genes, and modulated metabolic enzymes by downregulating Phase I genes (CYP1A2, CYP3A11) while upregulating the Phase II gene GSTA3. Notably, DB upregulated AFB1-suppressed Nrf2 and its downstream targets (HO-1, NQO1, SOD1, GCLC, GCLM, GSS). DB also reversed AFB1-induced mitochondrial damage, including swelling and cristae disruption, and inhibited apoptosis by restoring Bcl-2 and reducing p53, Bax, Cyt-c, caspase-9, and caspase-3 expression. These findings suggest that DB protects against AFB1-induced liver injury by regulating oxidative stress, inflammation, apoptosis, and metabolic enzymes, suggesting it has significant potential as a therapeutic strategy for aflatoxin-related hepatic disorders.