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Curcumin Protects Human Trophoblast HTR8/SVneo Cells from H2O2-Induced Oxidative Stress by Activating Nrf2 Signaling Pathway

机译:姜黄素通过激活Nrf2信号通路保护人类滋养细胞HTR8 / SVneo细胞免受H2O2诱导的氧化应激。

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摘要

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 O -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 O for another 24 h. The results showed that H O 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 O -induced oxidative stress by activating Nrf2 signaling pathway.
机译:妊娠并发症与胎盘中滋养细胞ROS积累引起的氧化应激有关。我们采用了人类滋养细胞HTR8 / SVneo细胞系来确定姜黄素预处理对HTR诱导的HTR8 / Sveo细胞氧化损伤的作用。将细胞用2.5或5μM姜黄素预处理24小时,然后再与400μMH O孵育24小时。结果表明,H O降低了HTR8 / Sveo细胞的细胞活力并诱导了活性氧(ROS)的过度积累。姜黄素预处理可通过增加Bcl-2 / Bax比并降低裂解半胱氨酸蛋白酶3的蛋白表达水平来有效保护HTR8 / SVneo细胞免受氧化应激诱导的细胞凋亡。抗氧化酶的活性。姜黄素的抗氧化作用是通过激活Nrf2及其下游抗氧化蛋白来实现的。另外,通过Nrf2-siRNA转染敲低Nrf2消除了姜黄素对HTR8 / SVneo细胞抗氧化损伤的保护作用。两者合计,我们的结果表明姜黄素可以通过激活Nrf2信号通路来保护HTR8 / SVneo细胞免受H O诱导的氧化应激。

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