Tumor Necrosis Factor-α Induced Cellular Stress on Trophoblastic Cells: NF-κB Signaling Could be a Potential Therapeutic Target

Objective: The development of the human placenta depends on proliferation and differentiation trophoblastic cells. Deficiencies in functions are known to have a critical role progression placental pathologies such as preeclampsia. Therefore, this research, it was aimed evaluate responses cells tumor necrosis factor-α (TNF-α) mediated cellular stress. Materials Methods: In study, stress model set up by treating JAR with 100ng/ml TNF-α for 1, 6, 12 24 hour long periods. model, effects capacity apoptotic activity were investigated immunocytochemistry. nuclear total expression levels factor-κB (NF-κB) evaluated immunocytochemistry Western blot, respectively. Results: It shown that 100 ng/ml treated had reduced proliferative increased immunocytochemical staining PCNA caspase-8 proteins respect, NF-κB signaling pathway plays induced processes. So that, group expressions compared untreated one. Conclusion: Our findings showed has significant source stimulated response could be defined decreased capacity, syncytiotrohoblastic cell lines. investigation related especially is further required understanding mechanism which crucial therapeutic approaches.