53 Magnesium sulfate affords neuroprotection in an eclampsia-like model induced in pregnant rats by ameliorating brain edema and neuroinflammation: Immune and inflammatory mechanisms
详细信息    查看全文
  • 作者:Xiaolan Li ; Xinjia Han ; Huishu Liu
  • 刊名:Pregnancy Hypertension: An International Journal of Women's Cardiovascular Health
  • 出版年:2016
  • 出版时间:July 2016
  • 年:2016
  • 卷:6
  • 期:3
  • 页码:162
  • 全文大小:38 K
文摘
Eclampsia is defined as the onset of grand mal seizures on the basis of preeclampsia. Presently, magnesium sulfate (MgSO4) is the most effective drug in treating elcamptic seizure, but the mechanism how (MgSO4) prevents eclampsia is still unclear.

Objectives

The aim of the present study was to investigate the neuroprotective effects of (MgSO4) on an eclampsia-like seizure model and explore the related mechanism.

Methods

We investigated the effects of (MgSO4) on brain edema, neuronal loss and neuroinflammation following pentylenetetrazol-induced eclampsia-like seizure in a rat model of preeclampsia. Brain water content was measured for assessing brain edema; enzyme-linked immunosorbent assay was used for detecting the cerebrospinal fluid levels of S100-B and Ferritin which are associated with neuroinflammation; nissl staining was used for detecting neuronal loss in the hippocampal CA1 region (CA1), immunofluorescence staining of Iba-1 and GFAP was used for detecting the density of microglia and astrocytes in the CA1 area.

Results

Our results revealed that (MgSO4) effectively attenuated brain edema, and significantly decreased the cerebrospinal fluid levels of S100-B and Ferritin; Furthermore, MgSO4 statistically ameliorated neuronal loss in the hippocampal CA1 area and inhibited the increase of microglia and astrocytes following eclampsia-like seizure.

Conclusions

Magnesium sulfate administration prevented neuronal loss in our rat model of eclampsia possiblely by causing a reduction in brain edema and neuroinflammation.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700