Synergistic effects of bioactive peptide and cytarabine on leukemia cells

Purpose Acute leukemia is caused by the malignant cloning of primitive bone marrow naive cells in vivo. This study aimed to explore the effects of anti-cancer bioactive peptides (ACBP) on leukemia cell proliferation, apoptosis, and peripheral blood lymphocytes in leukemia mice and to assess the combined effects of ACBP and the chemotherapy drug cytarabine (Ara-C) on acute leukemia. Materials and methods Cell proliferation and viability were measured using CCK-8. Apoptosis and cell cycle were measured by flow cytometry, and Caspase 3/7 protein expression was measured using an IncuCyte Live cell workstation. BALB/c mice were inoculated intraperitoneally to establish a P388 acute lymphatic leukemia cell model. Mouse peripheral blood lymphocyte subsets (Th, Ts, B, and NK cells) were detected by flow cytometry after ACBP, Ara-C, and ACBP/Ara-C treatment, and the levels of cytokines (TNF-α, IFN-r, IL-2, IL-4, IL-6, and IL-10) were also assessed. Results The results showed that ACBP effectively inhibited the proliferation of human myeloid leukemia mononuclear (THP-1) cells. The combined regimen also significantly induced apoptosis in THP-1 cells, upregulated Caspase3/7 expression, and blocked cell cycle in G2/M phase. Further ACBP/Ara-C activated Th, Ts, and B cells in P388 leukemic mice, upregulated of IFN-r and IL-2, downregulation of TNF- α, and IL-6. Conclusion These findings suggest that ACBP inhibits leukemia cell proliferation by activating the Caspase 3/7 pathway, arresting the cell cycle, activating lymphocyte subsets, promoting the secretion of cytokines, and activating immune functions. The synergistic effects of ACBP and Ara-C present new options for the clinical treatment of leukemia.