<p><i>Volvariella volvacea</i> is an edible and medicinal fungus; however, its hepatoprotective effects have not been reported. In this study, we evaluated the hepatoprotective effects of <i>V. volvacea</i> polysaccharides (SMP) by constructing a cellular model of H<sub>2</sub>O<sub>2</sub>-induced oxidative damage and an animal model of tetrachloromethane (CCl<sub>4</sub>)-induced acute liver injury in mice. Moreover, we used ML385, a specific Nrf2 blocker, to explore how SMP might regulate the Nrf2 signaling pathway. SMP is a primarily glucose-based polysaccharide with antioxidant capacities. In vitro analyses revealed that the administration of SMP significantly activated Nrf2, upregulated the expression of HO-1 and NQO1, enhanced SOD and CAT enzyme activities, and attenuated reactive oxygen species in H₂O₂-injured hepatocytes. In vivo, SMP reduced the serum levels of ALT, TNF-α, IL-6, and MDA while increasing the activity of hepatic SOD and ameliorating CCl₄-induced histopathology. Our findings revealed that SMP acts via a dual mechanism involving Nrf2-mediated antioxidant pathway activation coupled with NF-κB inflammatory signaling suppression. Collectively, our findings provide a pharmacological foundation for the therapeutic application of SMP in hepatoprotection.</p>

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Volvariella volvacea polysaccharides alleviate acute liver injury by modulating Nrf2/NF-κB pathway in a dual manner

  • Xiaomin Li,
  • Fengpei Zhang,
  • Yun Li,
  • Jiarong Cai,
  • Linna Cai,
  • Qianying Ren,
  • Anyan Fan,
  • Baisheng Xu,
  • Junsheng Fu

摘要

Volvariella volvacea is an edible and medicinal fungus; however, its hepatoprotective effects have not been reported. In this study, we evaluated the hepatoprotective effects of V. volvacea polysaccharides (SMP) by constructing a cellular model of H2O2-induced oxidative damage and an animal model of tetrachloromethane (CCl4)-induced acute liver injury in mice. Moreover, we used ML385, a specific Nrf2 blocker, to explore how SMP might regulate the Nrf2 signaling pathway. SMP is a primarily glucose-based polysaccharide with antioxidant capacities. In vitro analyses revealed that the administration of SMP significantly activated Nrf2, upregulated the expression of HO-1 and NQO1, enhanced SOD and CAT enzyme activities, and attenuated reactive oxygen species in H₂O₂-injured hepatocytes. In vivo, SMP reduced the serum levels of ALT, TNF-α, IL-6, and MDA while increasing the activity of hepatic SOD and ameliorating CCl₄-induced histopathology. Our findings revealed that SMP acts via a dual mechanism involving Nrf2-mediated antioxidant pathway activation coupled with NF-κB inflammatory signaling suppression. Collectively, our findings provide a pharmacological foundation for the therapeutic application of SMP in hepatoprotection.