Efficacy of Low Molecular Heparin on Preeclampsia by Inhibiting Apoptosis of Trophoblasts via the p38MAPK Signaling Pathway

Abstract

Objective. To explore the efficacy of low molecular heparin on preeclampsia by inhibiting apoptosis of trophoblasts via the p38MAPK signaling pathway. Methods. A preeclampsia rat model was established, and the effects of low molecular heparin on preeclampsia via the p38MAPK signaling pathway were analyzed based on intervention of the rats with different combinations of low molecular heparin and p38MAPK signaling pathway activator. Furthermore, a hypoxia/reoxygenation model of trophoblasts in vitro was established to explore the effects of low molecular heparin on trophoblasts via the p38MAPK signaling pathway. Results. After treatment with low molecular heparin, pregnant rats in the heparin group showed significantly decreased blood pressure, 24 h proteinuria, and p38MAPK protein levels in placenta tissues and decreased apoptosis rate of placenta tissue cells (all P < 0.05 ) and showed more fetal rats and lowered weight of them (both P < 0.05 ) but showed no significant change in the weight of placenta (all P > 0.05 ). Pregnant rats treated with low molecular heparin and p38MAPK activator showed significantly higher blood pressure, 24 h proteinuria, and p38MAPK protein levels in placenta tissues and apoptosis rate of placenta tissue cells than those of pregnant rats in the heparin group (all P < 0.05 ) and also showed less fetal rats and lighter fetal rats than those in the heparin group (both P < 0.05 ) but showed no difference with them in the weight of placenta ( P > 0.05 ). Further analysis revealed that low molecular heparin could protect the survival and migration of trophoblasts under hypoxia/reoxygenation conditions and reduce apoptosis of them (all P < 0.05 ). Conclusion. Low molecular heparin can alleviate preeclampsia by inhibiting the p38MAPK signaling pathway and can inhibit apoptosis of trophoblasts and promote proliferation and migration of them.

Expression and significance of cathepsin C and cathepsin D during pregnancy and Preeclampsia

“…It has been documented that women with PE have impaired uterine decidua [ 23 ]; hypoxia/reoxygenation injury promotes Cat C expression and activation of the p38MAPK/NF-κB pathway in human umbilical vein endothelial cells, but downregulation of Cat C inhibits p38MAPK/NF-κB pathway activation and increases vascular endothelial cell activity, such as enhancing endothelial cell invasion, anti-apoptosis, antioxidant capacity and angiogenic potential [ 24 ]. The p38MAPK signaling pathway regulates apoptosis and oxidative stress in endothelial cells in PE and affects the angiogenic activity of extravillous trophoblasts; hyperactivation of the p38MAPK pathway can lead to a variety of diseases, such as PE [ 9 , 10 ]. As a classical inflammatory and oxidative stress signaling pathway, the NF-κB pathway can lead to endothelial stress, uteroplacental dysfunction, and PE [ 11 , 12 ].…”

Chitosan‐Low Molecular Weight Heparin Sodium Nanoparticles Regulate Treg/Th17 Immune Balance and Inflammation at the Maternal‐Fetal Interface to Ameliorate Pre‐Eclampsia by HB‐EGF

“…[ 11 ] LMWH relieved pre‐eclampsia by inhibiting the p38MAPK signaling pathway, inhibiting trophoblast apoptosis, and promoting proliferation and migration. [ 12 ] LMWH combined with magnesium sulfate reduced trophoblast infiltration and ameliorated maternal hemagglutination in severe pre‐eclampsia patients. [ 13 ] Interestingly, the anti‐apoptotic effect of the Heparin‐binding epidermal growth factor (HB‐EGF) is a key factor for trophoblast survival.…”

Retracted: Efficacy of Low Molecular Heparin on Preeclampsia by Inhibiting Apoptosis of Trophoblasts via the p38MAPK Signaling Pathway

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Peer-review manipulation …”

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [1]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process:…”