open access

Vol 88, No 7 (2017)
Research paper
Published online: 2017-07-31
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Study of the relationship between AGEs and oxidative stress damage to trophoblast cell mitochondria

Lingling Jiang1, Jianying Yan1, Lixiang Wu1
DOI: 10.5603/GP.a2017.0070
·
Pubmed: 28819942
·
Ginekol Pol 2017;88(7):372-378.
Affiliations
  1. Fujian Provincial Maternity and Children’s Hospital of Fujian Medical University, Fuzhou, Fujian, China, China

open access

Vol 88, No 7 (2017)
ORIGINAL PAPERS Obstetrics
Published online: 2017-07-31

Abstract

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.

Abstract

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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Keywords

pre-eclampsia, advanced glycation end products, oxidative stress, trophoblast cell

About this article
Title

Study of the relationship between AGEs and oxidative stress damage to trophoblast cell mitochondria

Journal

Ginekologia Polska

Issue

Vol 88, No 7 (2017)

Article type

Research paper

Pages

372-378

Published online

2017-07-31

DOI

10.5603/GP.a2017.0070

Pubmed

28819942

Bibliographic record

Ginekol Pol 2017;88(7):372-378.

Keywords

pre-eclampsia
advanced glycation end products
oxidative stress
trophoblast cell

Authors

Lingling Jiang
Jianying Yan
Lixiang Wu

References (15)
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