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<p>Aflatoxin B1 (AFB1)–driven oxidative stress and apoptosis are central to hepatocellular carcinoma, yet cytoprotective nutraceutical matrices remain underexplored. We evaluated whether pomegranate (Punica granatum) seed oil (PSO), a punicic acid–rich lipid fraction, mitigates early AFB1 toxicity in HepG2 cells. Cells were allocated to control, PSO (8 µL/mL), AFB1 (20 ng/mL), or co-treatment for 16&#xa0;h. Mitochondrial metabolic activity (MTT), total antioxidant capacity (TAC), Annexin V/PI–resolved cell-death profiles, and caspase-3 (C3) and caspase-9 (C9) transcripts (RT-qPCR, 2⁻ΔΔCt) were quantified. AFB1 reduced viability to 88.9 ± 5.2% and TAC to 0.46 ± 0.08, expanded apoptotic/necrotic subpopulations (viable 44.2%; PI⁺ necrotic 6.9%), and upregulated C3 and C9 to 2.47 ± 0.38- and 2.81 ± 0.45-fold versus control (<i>p</i> &lt; 0.001). PSO alone was non-cytotoxic (101.5 ± 4.9% viability), increased TAC (1.27 ± 0.09; <i>p</i> &lt; 0.01), and down-modulated basal C3 and C9 (≈ 0.6-fold). Co-treatment partially rescued viability (92.7 ± 5.6%; <i>p</i> &lt; 0.01 vs. AFB1), normalized TAC (0.98 ± 0.06; NS vs. control), reduced PI⁺ necrosis (3.5%), and restored C3 and C9 transcripts to near-baseline (1.12 ± 0.21 and 1.18 ± 0.22; NS vs. control, <i>p</i> &lt; 0.001 vs. AFB1). These data demonstrate that PSO confers acute, redox-buffered, caspase-modulating cytoprotection against AFB1 in HepG2 cells without abolishing apoptosis, supporting PSO as a punicic-acid–dominant lipid matrix that moderates AFB1-driven redox collapse and excessive caspase transcript priming while preserving apoptosis surveillance, warranted for follow-on in-vivo validation, without implying enzymatic blockade or chronic therapeutic efficacy.</p>

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Punica Granatum Seed Oil Mitigates Aflatoxin B1–induced Oxidative Stress and Caspase-associated Apoptosis in HepG2 Cells

  • 期刊论文

  • 发表日期：

    2026年5月29日

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  • Ali Reza Khosravi,
  • Negar Hemmati,
  • Jalil Mehrzad

摘要

Aflatoxin B1 (AFB1)–driven oxidative stress and apoptosis are central to hepatocellular carcinoma, yet cytoprotective nutraceutical matrices remain underexplored. We evaluated whether pomegranate (Punica granatum) seed oil (PSO), a punicic acid–rich lipid fraction, mitigates early AFB1 toxicity in HepG2 cells. Cells were allocated to control, PSO (8 µL/mL), AFB1 (20 ng/mL), or co-treatment for 16 h. Mitochondrial metabolic activity (MTT), total antioxidant capacity (TAC), Annexin V/PI–resolved cell-death profiles, and caspase-3 (C3) and caspase-9 (C9) transcripts (RT-qPCR, 2⁻ΔΔCt) were quantified. AFB1 reduced viability to 88.9 ± 5.2% and TAC to 0.46 ± 0.08, expanded apoptotic/necrotic subpopulations (viable 44.2%; PI⁺ necrotic 6.9%), and upregulated C3 and C9 to 2.47 ± 0.38- and 2.81 ± 0.45-fold versus control (p < 0.001). PSO alone was non-cytotoxic (101.5 ± 4.9% viability), increased TAC (1.27 ± 0.09; p < 0.01), and down-modulated basal C3 and C9 (≈ 0.6-fold). Co-treatment partially rescued viability (92.7 ± 5.6%; p < 0.01 vs. AFB1), normalized TAC (0.98 ± 0.06; NS vs. control), reduced PI⁺ necrosis (3.5%), and restored C3 and C9 transcripts to near-baseline (1.12 ± 0.21 and 1.18 ± 0.22; NS vs. control, p < 0.001 vs. AFB1). These data demonstrate that PSO confers acute, redox-buffered, caspase-modulating cytoprotection against AFB1 in HepG2 cells without abolishing apoptosis, supporting PSO as a punicic-acid–dominant lipid matrix that moderates AFB1-driven redox collapse and excessive caspase transcript priming while preserving apoptosis surveillance, warranted for follow-on in-vivo validation, without implying enzymatic blockade or chronic therapeutic efficacy.