Journal
GINEKOLOGIA POLSKA
Volume 88, Issue 7, Pages 372-378Publisher
VIA MEDICA
DOI: 10.5603/GP.a2017.0070
Keywords
pre-eclampsia; advanced glycation end products; oxidative stress; trophoblast cell
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Funding
- Natural Science Foundation of Fujian Province of China [2012J01313]
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Objectives: To study the influence of AGEs on placental trophoblast mitochondria oxidative stress, and to explore the possible pathogenesis which may participate in pre-eclampsia. Material and methods: Human trophoblast cells from early pregnancy were cultured by an enzyme-digestion method. When trophoblast cells reached approximately 70-80% after passages, they were incubated with pre-eclampsia serum for 24 hours. A fluorescent dye assay was applied to measure the mitochondrial membrane potential; ELISA was used to measure the activity of the mitochondrial permeability transition pore. mtDNA was detected by Real-time fluorescence quantitative Reverse Transcription-Polymerase Chain Reaction (RT-PCR). We continued to culture one group of cells with pre-eclampsia maternal serum, and other cells were pulsed with 600 mg/L AGEs. Cells were incubated for 16 hours before assaying the levels of mitochondrial oxidative stress damage. Results: The levels of mitochondria oxidative stress damage in the AGEs group were higher than in the pre-eclampsia group 1 and pre-eclampsia group 2. There was no statistically significant difference in mitochondrial oxidative stress damage between the pre-eclampsia group 1 and group 2. Conclusions: The AGEs are involved in the pathogenesis of pre-eclampsia, possibly through the enhancement of mitochondrial oxidative stress damage.
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