Fenbendazole, is an effective
benzimidazole anthelmintic that prevents
parasite infection in both human and veterinary health care. Although the well-known and effect of
benzimidazole was recently shown to have a broad spectrum of biological abilities, such as anticancer and anti-
inflammation activities, the mechanism of
benzimidazole's antiproliferative effect via cell signaling pathways and its role in preimplantation has not been studied. Therefore, the purpose of this study was to determine the effects of
fenbendazole on porcine trophectoderm and
luminal epithelial cells. First, we investigated cell viability in response to a low dose of
fenbendazole, which highly inhibited cell proliferation. In addition, we investigated apoptotic molecules in the mitochondria, imbalanced intracellular
calcium homeostasis, and the expression of some genes involved in apoptosis to explain the decrease in proliferation. Finally, we examined the intracellular mechanisms of
fenbendazole by measuring the
extracellular signal-regulated kinase, PI3K/AKT, and
c-Jun N-terminal kinase signaling
proteins by western blot analysis. Our findings suggest that
fenbendazole functions as an effective anti-proliferative molecule that induces critical apoptosis in the porcine trophectoderm and uterine
luminal epithelial cells by disrupting the mitochondria membrane potential during early pregnancy.