Abstract:
:Pregnancy complications are associated with abnormal cytotrophoblast differentiation and invasion. Hydrogen peroxide (H2O2) is an important mediator of oxidative ischemia/reperfusion stress in the placenta. Lycium barbarum polysaccharides (LBP) have been demonstrated to counteract oxidative free radicals. The effects of LBP in trophoblast HTR8/SVneo cells injured with H2O2 were examined. A cell counting kit‑8 assay was performed to detect the effect of LBP at different concentrations on the proliferative ability of H2O2 injured trophoblast cells. Flow cytometry was used to determine the levels of reactive oxygen species (ROS), mitochondria membrane potential (MMP) disruption and apoptosis. Superoxide dismutase (SOD) activity and lactate dehydrogenase (LDH) leakage into the supernatant was detected by ultraviolet spectrophotometry. Reverse transcription‑quantitative polymerase chain reaction and western blot analysis were performed to detect the expression of apoptosis‑associated factors, including survivin, hypoxia inducible factor 1‑α (HIF1‑α), Bcl‑2 apoptosis regulator (Bcl‑2), Bcl‑2 associated X apoptosis regulator (Bax). The results revealed that LBP protected the proliferative ability of trophoblast cells injured with H2O2 in a dose‑dependent manner. LBP inhibited the oxidative stress induced by H2O2, by reducing ROS and LDH levels and increasing SOD activity. Additionally, LBP decreased MMP disruption and cell apoptosis induced by H2O2, by increasing the mRNA and protein expression of survivin, HIF1‑α and Bcl‑2 and decreasing Bax expression. Therefore, it was concluded that LBP protected human trophoblast cells from H2O2‑induced oxidative stress and cell apoptosis via regulation of apoptosis‑associated factor expression. It will provide a novel strategy for the treatment of pregnancy complications.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Li J,Ding Z,Yang Y,Mao B,Wang Y,Xu Xdoi
10.3892/mmr.2018.9274subject
Has Abstractpub_date
2018-09-01 00:00:00pages
2581-2588issue
3eissn
1791-2997issn
1791-3004journal_volume
18pub_type
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