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姜黄素通过激活Nrf2信号通路保护人滋养层HTR8/SVneo细胞免受HO诱导的氧化应激。

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

作者信息

Qi Lina, Jiang Jingle, Zhang Jingfei, Zhang Lili, Wang Tian

机构信息

National Experimental Teaching Demonstration Center of Animal Science, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.

出版信息

Antioxidants (Basel). 2020 Feb 1;9(2):121. doi: 10.3390/antiox9020121.

DOI:10.3390/antiox9020121
PMID:32024207
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7071057/
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 HO-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 HO for another 24 h. The results showed that HO 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 HO-induced oxidative stress by activating Nrf2 signaling pathway.

摘要

妊娠并发症与胎盘滋养层活性氧(ROS)积累所诱导的氧化应激相关。我们采用人滋养层HTR8/SVneo细胞系来确定姜黄素预处理对HTR8/Sveo细胞中过氧化氢(HO)诱导的氧化损伤的影响。细胞用2.5或5μM姜黄素预处理24小时,然后再用400μM HO孵育24小时。结果表明,HO降低了HTR8/Sveo细胞的活力并诱导活性氧(ROS)过度积累。姜黄素预处理通过增加Bcl-2/Bax比值和降低裂解型半胱天冬酶3的蛋白表达水平,有效保护HTR8/SVneo细胞免受氧化应激诱导的凋亡。此外,姜黄素预处理通过增强抗氧化酶的活性减轻了过度的氧化应激。姜黄素的抗氧化作用是通过激活核因子E2相关因子2(Nrf2)及其下游抗氧化蛋白实现的。此外,通过Nrf2-siRNA转染敲低Nrf2消除了姜黄素对HTR8/SVneo细胞氧化损伤的保护作用。综上所述,我们的结果表明姜黄素可通过激活Nrf2信号通路保护HTR8/SVneo细胞免受HO诱导的氧化应激。

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