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硫酸镁可在人胎盘体外模型中预防脂多糖诱导的细胞死亡。

Magnesium sulphate prevents lipopolysaccharide-induced cell death in an in vitro model of the human placenta.

作者信息

Williamson Rachel D, McCarthy Cathal, Kenny Louise C, O'Keeffe Gerard W

机构信息

Irish Centre for Fetal and Neonatal Translational Research (INFANT), Cork University Maternity Hospital, Cork, Ireland; Department of Obstetrics and Gynaecology, Cork University Maternity Hospital, Cork, Ireland.

Irish Centre for Fetal and Neonatal Translational Research (INFANT), Cork University Maternity Hospital, Cork, Ireland; Department of Obstetrics and Gynaecology, Cork University Maternity Hospital, Cork, Ireland.

出版信息

Pregnancy Hypertens. 2016 Oct;6(4):356-360. doi: 10.1016/j.preghy.2016.08.237. Epub 2016 Aug 30.

Abstract

OBJECTIVES

To determine if magnesium sulphate (MgSO) prevents lipopolysaccharide (LPS)-induced cell death in an in vitro model of the human placenta.

STUDY DESIGN

BeWo choriocarcinoma cells were treated with increasing concentrations of LPS (10-1000ng/ml) and MgSO ranging from 1 mM to 100 mM for 24 or 48h. For co-treatments, cells were pre-treated with 1mM MgSO for 1h and 200ng/ml LPS was then added for the remaining 48h. To assess viability an MTT assay was carried out along with nuclear staining to assess pyknotic nuclei. The expression of the pro-inflammatory cytokine TNF-α was examined by real-time PCR.

RESULTS

MgSO had a dose dependent effect of cell viability with a narrow therapeutic window. MgSO (1mM) protected against adverse effects of LPS on cell viability by preventing LPS-induced decreases in cell viability (MTT assay) and protecting against LPS-induced pyknotic changes in nuclear membrane. MgSO also inhibited the elevated TNF-α mRNA expression induced by LPS.

CONCLUSIONS

MgSO preserves BeWo cell viability following an inflammatory insult and reduces the mRNA expression of the inflammatory cytokine TNF-α. These data elucidate a potential therapeutic pathway by which MgSO may be protective in pre-eclampsia.

摘要

目的

在人胎盘体外模型中确定硫酸镁(MgSO)是否能预防脂多糖(LPS)诱导的细胞死亡。

研究设计

将BeWo绒毛膜癌细胞用浓度递增的LPS(10 - 1000ng/ml)和浓度范围为1mM至100mM的MgSO处理24或48小时。对于联合处理,细胞先用1mM MgSO预处理1小时,然后加入200ng/ml LPS处理剩余的48小时。通过MTT试验评估细胞活力,并进行核染色以评估固缩核。通过实时PCR检测促炎细胞因子TNF-α的表达。

结果

MgSO对细胞活力具有剂量依赖性作用,且治疗窗较窄。MgSO(1mM)通过防止LPS诱导的细胞活力下降(MTT试验)以及防止LPS诱导的核膜固缩变化,保护细胞免受LPS的不利影响。MgSO还抑制了LPS诱导的TNF-α mRNA表达升高。

结论

MgSO在炎症损伤后可维持BeWo细胞活力,并降低炎性细胞因子TNF-α的mRNA表达。这些数据阐明了MgSO在子痫前期可能具有保护作用的潜在治疗途径。

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