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.
Bibliographical noteFunding Information:
This research was supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute funded by the Ministry of Health and Welfare (grant number: HI17C0929 ) and the National Research Foundation of Korea (NRF) grant funded by the Ministry of Science and ICT (MSIT) (No. 2018R1C1B6009048 ).
Copyright 2019 Elsevier B.V., All rights reserved.
- Apoptotic factors
- Porcine cells
ASJC Scopus subject areas
- Environmental Engineering
- Environmental Chemistry
- Waste Management and Disposal