The role of resveratrol in cervical cancer in apoptosis

Cancer is one of the types of diseases that occur as a result of the normal genes being mutated and their functions impaired or completely lost. Cervical cancer is the second most common type of cancer among women and poses a great threat to women's health. Chemotherapeutic agents are biochemical compounds that change the biochemical processes of cells, prevent the proliferation of cells directly or indirectly, and are used to control symptoms such as suppressing tumor development. Cisplatin is a chemotherapeutic agent that is frequently applied against many types of cancer such as uterine, breast, testicular and brain cancer. Resveratrol (RSV), a natural antioxidant, is known to have antiproliferative and apoptotic effects on cancer cells. Many studies have also shown that the combined use of natural products and chemotherapy agents can increase the sensitivity and cytotoxicity of chemotherapy agents.In this thesis, the apoptotic effects of CDDP and RSV in combination on HeLa cervical cancer cells were discussed. MTT method was used to determine the cytotoxic effects of CDDP and RSV on HeLa cells. Based on the MTT results, the IC50 values of CDDP and RSV were calculated as 30±12 µM and 60±16 µM, respectively. Combinations of CDDP and RSV were formed based on the percentages of the IC50 values obtained, as combination 50 (KM50) (15 µM CDDP, 30 µM RSV) and combination 40 (KM40) (12 µM CDDP, 24 µM RSV). Apoptotic effects of CDDP, RSV and combinations on cells were determined by Annexin-V FITC/PI, caspase-9 methods. In the method studied with Annexin-V FITC, the group in which 60 µM RSV was applied to HeLa cell caused a higher rate of apoptosis than CDDP and combinations. Negative caspase-9 activity (83,8%) and positive caspase-9 activity (16,0%) were observed in HeLa cells.A decrease in the percentages of positive caspase-9 occurred in separate and combined treatments of CDDP and RSV. In conclusion, combinations of KM50 and KM40 containing low dose CDDP and RSV synergistically inhibited HeLa cell growth by inducing apoptotic death.