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This study aimed to evaluate the effects of Genistein, an isoflavone antioxidant found in soy, on liver cancer (HepG2) and healthy (HDF) cells by assessing its influence on antioxidant activity, cell viability, and CD36-mediated lipid transport. Cells were cultured and prepared for treatment. Cell viability was measured using the MTT assay. CD36 levels were quantified with a CD36 ELISA kit. Antioxidant parameters—including SOD, GSH, MDA, MPO, and GPx—were analyzed using corresponding biochemical assays. Genistein treatment (6.25–200 μg/mL, 48 h) showed a dose-dependent reduction in HepG2 cell viability. Although low concentrations (6.25–25 μg/mL) did not reduce viability below 50%, higher concentrations (50–200 μg/mL) demonstrated significant anticancer activity, decreasing viability below 50% (IC50: 35.34 ± 0.924 μg/mL). Methotrexate (MTX), used as a positive control, showed a similar pattern with an IC50 of 24.35 ± 0.681 μg/mL. ELISA results revealed that Genistein more effectively increased CD36 expression in HepG2 cells compared to MTX (p=0.002) and the control (p<0.001). MTX also showed increased CD36 expression versus control (p<0.001). In HDF cells, both Genistein (p=0.002) and MTX (p=0.048) elevated CD36 levels relative to control.
Antioxidant analyses showed that MTX significantly elevated MDA levels in HepG2 cells (p=0.031), whereas Genistein significantly increased GPx levels in HDF cells (p<0.001*). Genistein exhibits therapeutic potential in HepG2 liver cancer cells. It modulates CD36 and MDA expression, reducing lipid accumulation, while in HDF cells it affects CD36 and GPx activity. These findings suggest that Genistein may contribute to lipid regulation and oxidative balance in both cancerous and healthy cells.
| Keywords | cancer, liver, phenolic compound, CD36, lipids |
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