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Pretreatment of artesunate promoted hepatocyte proliferation by activating the PI3K/Akt/mTOR signaling pathway in mice

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  • Additional Information
    • Publication Information:
      Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia, 2024.
    • Publication Date:
      2024
    • Collection:
      LCC:Surgery
    • Abstract:
      ABSTRACT Purpose: Artesunate (ART) has been implicated in regulating the many processes of liver injury, but its roles in liver regeneration still need to be illustrated. Methods: In the present study, ART was used to pretreat hepatocyte cell line NCTC1469 to study the effect of ART on hepatocyte proliferation in vitro. Furthermore, the potency of ART as a regimen to promote liver regeneration and restore liver function was evaluated following partial hepatectomy (PH) on C57BL/6 mice. Results: ART concentration-dependently promoted hepatocyte proliferation and reduced apoptosis. Cell cycle and Ki-67 immunohistochemical analyses demonstrated that ART supplementation promoted the proliferation of hepatocytes and accelerated liver regeneration. Our results provided evidence that ART improved liver function in a dose-dependent manner, as indicated by decreased serum alanine aminotransferase, aspartate aminotransferase, and increased albumin, and hepatocyte growth factor levels in PH mice. Meanwhile, ART promoted the PI3K/Akt/mTOR signaling in NCTC1469 cells and liver tissue of PH mice. In addition, PI3K inhibitor LY294002 blocked the promotion effect of ART on hepatocyte proliferation and cell cycle progression. Conclusion: ART promoted hepatocyte proliferation via activation of the PI3K/Akt/mTOR pathway, which was beneficial to liver regeneration of PH-induced liver injury.
    • File Description:
      electronic resource
    • ISSN:
      1678-2674
    • Relation:
      http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502024000100254&lng=en&tlng=en; http://www.scielo.br/pdf/acb/v39/1678-2674-acb-39-e394324.pdf; https://doaj.org/toc/1678-2674
    • Accession Number:
      10.1590/acb394324
    • Accession Number:
      edsdoj.92df001ccfe443d7aaaaeb8631a15ee7