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Curcumin Protects Human Trophoblast HTR8/SVneo Cells from H(2)O(2)-Induced Oxidative Stress by Activating Nrf2 Signaling Pathway

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 H(2)O(2)-induced oxidative damage in HTR8/Sveo cells. Cells were pret...

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Detalles Bibliográficos
Autores principales: Qi, Lina, Jiang, Jingle, Zhang, Jingfei, Zhang, Lili, Wang, Tian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7071057/
https://www.ncbi.nlm.nih.gov/pubmed/32024207
http://dx.doi.org/10.3390/antiox9020121
Descripción
Sumario: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 H(2)O(2)-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 H(2)O(2) for another 24 h. The results showed that H(2)O(2) 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 H(2)O(2)-induced oxidative stress by activating Nrf2 signaling pathway.