Research Information System
Fabad Journal of Pharmaceutical Sciences, vol.50, no.2, pp.259-270, 2025 (Scopus, TRDizin)
This study evaluates the potential of epigallocatechin-3-gallate (EGCG) to mitigate 5-fluorouracil (5-FU)-induced hepatotoxicity using the AML-12 cell line. The AML-12 cell line is divided into four groups: control, 5-FU, EGCG, and 5-FU+EGCG. IC50 (Inhibitory Concentration 50) values are determined using the MTT assay. The mRNA expression levels of antioxidant system-related genes, including SOD, CAT, and GSH, are analyzed via RT-qPCR. Additionally, the expression levels of apoptosis-related genes such as Caspase-9 (Cas-9), Apaf-1, Caspase-3 (Cas-3), Bcl-2, and Bax, as well as p53 and SMAC/DIABLO, are evaluated. Co-administration of EGCG with 5-FU results in a significant increase in GSH, SOD, and CAT mRNA expression levels. Treatment with 5-FU alone significantly increases the expression levels of SMAC/ DIABLO, Bax, Apaf-1, Bcl-2, and Cas-3 mRNA by inducing apoptosis. Furthermore, co-administration of EGCG and 5-FU leads to a significant elevation in the mRNA expression levels of Cas-9, Bax, Apaf-1, p53, Cas-3, and SMAC/DIABLO, indicating the elimination of damaged structures through apoptosis. In conclusion, our findings demonstrate that EGCG exerts a hepatoprotective effect against 5-FU-induced damage through its antioxidant properties. Moreover, EGCG enhances the anticancer efficacy of 5-FU by promoting apoptosis and facilitating the removal of damaged cells. These results suggest a potential therapeutic synergy between EGCG and 5-FU in treating liver damage and cancer.