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[内毒素诱导牛肺动脉内皮细胞中过氧亚硝酸盐的生成]

[Endotoxin-induced generation of peroxynitrite in bovine pulmonary arterial endothelial cells].

作者信息

Gu Z Y, Ling Y L

机构信息

Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2001 Nov;17(4):379-82.

Abstract

AIM

To explore the significance of bovine pulmonary arterial endothelial cell (BPAEC) to produce peroxynitrite (ONOO-).

METHODS

The contents of nitrotyrosine (NT), a marker of ONOO- generation in vivo,were quantitatively measured with flow cytometric and immunofluorescent technique in cultured BPAEC induced by lipopolysaccharide (LPS), a major component of bacterial endotoxin. In addition, effect of ONOO- on micromorphologic features of BPAEC was observed.

RESULTS

LPS caused significant increase of NT in BPAEC in a dose-dependent manner, which was in part reversed by aminoguanidine, a selective inhibitor of inducible nitric oxide synthase. Exposure of BPAEC to exogenous ONOO- resulted in the cellular retro-contraction with diminished cellular body and increased width of cellular junction.

CONCLUSION

LPS may induce the ONOO- formation of BPAEC. Endothelial cell-derived ONOO- may mediate the deleterious effect of LPS on BPAEC per se.

摘要

目的

探讨牛肺动脉内皮细胞(BPAEC)产生过氧亚硝酸盐(ONOO-)的意义。

方法

采用流式细胞术和免疫荧光技术,定量检测培养的BPAEC中硝基酪氨酸(NT,体内ONOO-生成的标志物)的含量,该细胞由细菌内毒素的主要成分脂多糖(LPS)诱导。此外,观察了ONOO-对BPAEC微观形态特征的影响。

结果

LPS以剂量依赖的方式导致BPAEC中NT显著增加,诱导型一氧化氮合酶的选择性抑制剂氨基胍可部分逆转这一现象。BPAEC暴露于外源性ONOO-会导致细胞逆向收缩,细胞体缩小,细胞间隙宽度增加。

结论

LPS可能诱导BPAEC形成ONOO-。内皮细胞衍生的ONOO-可能介导LPS对BPAEC本身的有害作用。

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