Title Effects of mebendazole and semaglutide on oxidative stress in vitro using melanoma cell culture model
Translation of Title Mebendazolo ir semaglutido efektas oksidaciniam stresui in vitro melanomos ląstelių kultūrų modelyje.
Authors Ratkutė, Kamilė Atėnė
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Pages 47
Keywords [eng] melanoma, oksidacinis stresas, mebendazolas, semaglutidas, mebendazolo semaglutido derinys, ląstelių proliferacija, reaktyviosios deguonies formos, ROS, ląstelių migracija / melanoma, oxidative stress, mebendazole, semaglutide, mebendazole-semaglutide, cell proliferation, reactive oxygen species, ROS, cell migration.
Abstract [eng] Aim: to evaluate the effects of mebendazole, semaglutide and mebendazole-semaglutide combination on oxidative stress in an in vitro melanoma cell culture model SK-MEL-28. Objectives: 1. To evaluate the effects of mebendazole on melanoma cell proliferation, intracellular melanoma reactive oxygen species levels and melanoma cell migration in an in vitro melanoma cell culture model SK-MEL-28. 2. To evaluate the effects of semaglutide on melanoma cell proliferation, intracellular melanoma reactive oxygen species levels and melanoma cell migration in an in vitro melanoma cell culture model SK-MEL-28. 3. To evaluate the effects of mebendazole-semaglutide combination on melanoma cell proliferation, intracellular melanoma reactive oxygen species levels and melanoma cell migration in an in vitro melanoma cell culture model SK-MEL-28. 4. To perform a comparative analysis of the effects of mebendazole, semaglutide and mebendazole-semaglutide combination on melanoma cell proliferation, intracellular melanoma reactive oxygen species levels and melanoma cell migration in an in vitro melanoma cell culture model SK-MEL-28. Methods: In this study, spectrophotometric analysis, fluorometric intracellular reactive oxygen species assay and wound healing (scratch) assay were employed to investigate the experimental group effects on melanoma cell proliferation, intracellular melanoma reactive oxygen species levels and melanoma cell migration, respectively. Statistical data differences were assessed using either Student’s t-test, one-way Anova, or the non-parametric Kruskal-Wallis test, as appropriate; Tukey’s test was applied for multiple comparisons among experimental groups. Differences were considered statistically significant at p < 0.05. Results: Melanoma cell proliferation was inhibited by mebendazole 1 µM (p = 0.008) at 24 hours; by mebendazole 0.5 µM (p = 0.024) and mebendazole 0.1; 0.5; 1 µM-semaglutide 0.6 µM (p = 0.032; p = 0.005; p = 0.028, respectively) at 48 hours. Intracellular reactive oxygen species levels were significantly increased by semaglutide (p = 0.035) at 24 hours. Comparative analysis revealed significant differences between effects on melanoma cell proliferation of mebendazole 1 µM and semaglutide 0.6 µM at 24 hours; of semaglutide 0.6 µM and mebendazole 0.1; 0.5; 1 µM-semaglutide 0.6 µM at 48 hours. Differences were found between effects of mebendazole 0.5 µM and all other experimental groups on melanoma cell migration at 24 and 48 hours. Conclusions: Mebendazole 1 µM significantly inhibited melanoma cell proliferation at both 24 and 48 hours, while mebendazole 0.5 µM demonstrated significant antiproliferative effects at 48 hours. Semaglutide 0.6 µM significantly increased intracellular reactive oxygen species (ROS) levels at 24 hours. Mebendazole 0.1; 0.5; 1 µM-semaglutide 0.6 µM significantly reduced melanoma cell proliferation at 48 hours, with mebendazole 0.5 µM-semaglutide 0.6 µM producing the strongest antiproliferative effect. Comparative analysis revealed significant differences between semaglutide, mebendazole, and mebendazole–semaglutide combination effects on melanoma cell proliferation and migration.
Dissertation Institution Vilniaus universitetas.
Type Master thesis
Language English
Publication date 2026