Abstract
Pregnancy complications are associated with oxidative stress induced by accumulation of trophoblastic ROS in the placenta. We employed the human trophoblast HTR8/SVneo cell line to determine the effect of curcumin pre-treatment on H2O2-induced oxidative damage in HTR8/Sveo cells. Cells were pretreated with 2.5 or 5 μM curcumin for 24 h, and then incubated with 400 μM H2O2 for another 24 h. The results showed that H2O2 decreased the cell viability and induced excessive accumulation of reactive oxygen species (ROS) in HTR8/Sveo cells. Curcumin pre-treatment effectively protected HTR8/SVneo cells against oxidative stress-induced apoptosis via increasing Bcl-2/Bax ratio and decreasing the protein expression level of cleaved-caspase 3. Moreover, curcumin pre-treatment alleviated the excessive oxidative stress by enhancing the activity of antioxidative enzymes. The antioxidant effect of curcumin was achieved by activating Nrf2 and its downstream antioxidant proteins. In addition, knockdown of Nrf2 by Nrf2-siRNA transfection abolished the protective effects of curcumin on HTR8/SVneo cells against oxidative damage. Taken together, our results show that curcumin could protect HTR8/SVneo cells from H2O2-induced oxidative stress by activating Nrf2 signaling pathway.
Highlights
Intrauterine growth retardation (IUGR) and preeclampsia (PE) are detrimental pregnancy complications that could cause significant increased perinatal morbidity and mortality [1]
Knockdown of NFE2-related factor-2 (Nrf2) by Nrf2-Small Interfering RNA (siRNA) transfection abolished the protective effects of curcumin on HTR8/SVneo cells against oxidative damage
Our results show that curcumin could protect HTR8/SVneo cells from H2 O2 -induced oxidative stress by activating Nrf2 signaling pathway
Summary
Intrauterine growth retardation (IUGR) and preeclampsia (PE) are detrimental pregnancy complications that could cause significant increased perinatal morbidity and mortality [1]. IUGR refers to impaired growth and development of the fetus or fetal organs, and these consequences are associated with the dysfunction of placental trophoblast cells [3]. Oxidative stress arose from the production of reactive oxygen species (ROS) reduces the antioxidant capacity of cells, which, in turn, results in cell damage and eventually cell death [4,5]. The metabolisms of the mother and fetus are enhanced because of higher energy and oxygen requirements [6]. This could accelerate the accumulation of ROS, and eventually induce excessive oxidative stress in the trophoblast cells.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
