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[健康孕妇和先兆子痫孕妇中性粒细胞产生超氧阴离子的情况]

[Superoxide-anion production by neutrophil granulocytes in healthy and preeclamptic pregnant women].

作者信息

Lampé Rudolf

机构信息

DeOrvos- és Egészségtudományi Centrum Szülészeti és Nőgyógyászati Klinika és Megelőző Orovostani Intézet Debrecen Nagyerdei krt 98. 4032.

出版信息

Orv Hetil. 2012 Mar 18;153(11):425-34. doi: 10.1556/OH.2012.29322.

Abstract

Data on respiratory burst activity of granulocytes from healthy and preeclamptic pregnant women are contradictory. To further investigate a possible role of reactive oxygen species in the etiology of preeclampsia, the induced superoxide-anion generation by granulocytes from non-pregnant, healthy pregnant and preeclamptic pregnant women were measured. The reciprocal effects of heat-inactivated and non-inactivated plasma on superoxide production by neutrophils from non-pregnant, healthy pregnant and preeclamptic pregnant subjects were also examined. Superoxide generation was measured by ferricytochrome c reduction. Both phorbol-12.13-dibutirate- and N-formyl-methionyl-leucyl-phenylalanine-induced superoxide production was significantly decreased in normal pregnancy compared to results obtained in non-pregnant and preeclamptic pregnant women. Phorbol-12.13-dibutirate-induced superoxide generation by non-pregnant and preeclamptic neutrophils was significantly inhibited by heat-inactivated and non-inactivated healthy pregnant plasma. N-formyl-methionyl-leucyl-phenylalanine-stimulated superoxide production by non-pregnant and preeclamptic granulocytes was suppressed only by non-inactivated healthy pregnant plasma. Phorbol-12.13-dibutirate-induced superoxide generation of healthy pregnant neutrophils was significantly increased by inactivated and non-inactivated non-pregnant and preeclamptic plasma. N-formyl-methionyl-leucyl-phenylalanine-stimulated superoxide production by healthy pregnant granulocytes was significantly enhanced following treatment of the cells with non-inactivated non-pregnant and preeclamptic pregnant plasma. Deficient superoxide generation in normal pregnancy may be caused by maternal immunosuppressive factors. The failure of reduction in superoxide production in preeclampsia may be partly responsible for endothelial dysfunction. Apart from oxidative stress, a possible role of inefficient maternal immunosuppression should also be considered in the pathogenesis of preeclampsia.

摘要

关于健康孕妇和先兆子痫孕妇粒细胞呼吸爆发活性的数据相互矛盾。为了进一步研究活性氧在先兆子痫病因学中的可能作用,我们检测了非孕妇、健康孕妇和先兆子痫孕妇粒细胞诱导产生超氧阴离子的情况。同时还研究了热灭活和未灭活血浆对非孕妇、健康孕妇和先兆子痫孕妇中性粒细胞产生超氧的相互影响。通过高铁细胞色素c还原法测定超氧的产生。与非孕妇和先兆子痫孕妇相比,正常妊娠时佛波醇-12,13-二丁酸酯和N-甲酰甲硫氨酰亮氨酰苯丙氨酸诱导的超氧产生均显著降低。热灭活和未灭活的健康孕妇血浆均可显著抑制非孕妇和先兆子痫中性粒细胞由佛波醇-12,13-二丁酸酯诱导产生超氧。只有未灭活的健康孕妇血浆可抑制非孕妇和先兆子痫粒细胞由N-甲酰甲硫氨酰亮氨酰苯丙氨酸刺激产生超氧。灭活和未灭活的非孕妇及先兆子痫孕妇血浆均可显著增加健康孕妇中性粒细胞由佛波醇-12,13-二丁酸酯诱导产生超氧。用未灭活的非孕妇及先兆子痫孕妇血浆处理细胞后,健康孕妇粒细胞由N-甲酰甲硫氨酰亮氨酰苯丙氨酸刺激产生的超氧显著增强。正常妊娠中超氧产生不足可能是由母体免疫抑制因子引起的。先兆子痫中超氧产生未能降低可能部分导致了内皮功能障碍。除氧化应激外,母体免疫抑制效率低下在先兆子痫发病机制中也可能起作用。

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