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氙气在体外调节中性粒细胞黏附分子的表达。

Xenon modulates neutrophil adhesion molecule expression in vitro.

作者信息

de Rossi L W, Horn N A, Stevanovic A, Buhre W, Hutschenreuter G, Rossaint R

机构信息

University Hospital, Department of Anaesthesiology, Aachen, Germany.

出版信息

Eur J Anaesthesiol. 2004 Feb;21(2):139-43. doi: 10.1017/s0265021504002108.

DOI:10.1017/s0265021504002108
PMID:14977346
Abstract

BACKGROUND AND OBJECTIVE

Xenon reduces the infarct size after regional ischaemia in the rabbit heart in vivo, but the underlying mechanisms are unknown. Since adhesion molecules on neutrophils are closely involved in the pathophysiology of ischaemia/reperfusion injury and modulation of neutrophil function, we investigated the effect of xenon on neutrophil adhesion molecule expression in vitro.

METHODS

Freshly isolated neutrophils were incubated with 30% or 60% xenon for 60 min. In unstimulated and after stimulation with either N-formyl-methionyl-leucyl-phenylalanine or phorbol-12-myristate-13-acetate neutrophil surface expression of PSGL-1, L-selectin, CD11a and CD11b were measured by flow cytometry.

RESULTS

At both concentrations, xenon reduced the surface expression of PSGL-1 by 10% (P < 0.05), and of L-selectin by 15% (P < 0.05) in the 60% xenon group. Furthermore, N-formyl-methionyl-leucyl-phenylalanine activated neutrophils showed an increased removal of L-selectin from the neutrophil surface following incubation with xenon (30% compared to controls, P < 0.05). Neutrophil beta2-integrin expression was not altered by xenon.

CONCLUSIONS

Xenon increases the removal of the selectins PSGL-1 and L-selectin from the neutrophil surface in vitro. Since both selectins are involved in the initial contact between neutrophils and endothelial cells, xenon may affect neutrophil adhesion to endothelium during ischaemia/reperfusion injury. However, because the beta2-integrin expression was unaffected by xenon, further investigations are required to clarify whether xenon may modulate neutrophil transmigration through endothelial cells in vivo.

摘要

背景与目的

氙可减小家兔心脏局部缺血后的梗死面积,但具体机制尚不清楚。由于中性粒细胞上的黏附分子与缺血/再灌注损伤的病理生理学及中性粒细胞功能调节密切相关,我们在体外研究了氙对中性粒细胞黏附分子表达的影响。

方法

将新鲜分离的中性粒细胞与30%或60%的氙孵育60分钟。在未刺激以及用N-甲酰甲硫氨酰亮氨酰苯丙氨酸或佛波醇-12-肉豆蔻酸酯-13-乙酸酯刺激后,通过流式细胞术检测PSGL-1、L-选择素、CD11a和CD11b在中性粒细胞表面的表达。

结果

在两种浓度下,氙均可使60%氙组中PSGL-1的表面表达降低10%(P<0.05),L-选择素的表面表达降低15%(P<0.05)。此外,与氙孵育后,N-甲酰甲硫氨酰亮氨酰苯丙氨酸激活的中性粒细胞表面L-选择素的去除增加(与对照组相比为30%,P<0.05)。氙未改变中性粒细胞β2整合素的表达。

结论

氙在体外可增加中性粒细胞表面选择素PSGL-1和L-选择素的去除。由于这两种选择素均参与中性粒细胞与内皮细胞的初始接触,氙可能在缺血/再灌注损伤期间影响中性粒细胞与内皮的黏附。然而,由于β2整合素的表达不受氙的影响,需要进一步研究以阐明氙是否可在体内调节中性粒细胞通过内皮细胞的迁移。

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