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全氟碳化合物可防止肺微血管内皮细胞脂多糖诱导的细胞凋亡。

Perfluorocarbon Protects against Lipopolysaccharide-Induced Apoptosis of Endothelial Cells in Pulmonary Microvessels.

机构信息

Department of Respiratory Diseases, the First Medical Center, Chinese PLA General Hospital, Beijing, P.R. China.

Department of Respiratory Diseases, the First Hospital of Qinhuangdao, Qinhuangdao, P.R. China.

出版信息

Bull Exp Biol Med. 2021 Feb;170(4):410-414. doi: 10.1007/s10517-021-05077-8. Epub 2021 Mar 16.

Abstract

This study was aimed to explore the effect and mechanisms of action of perfluorocarbon on LPS-induced apoptosis of pulmonary microvascular endothelial cells (PMVEC) isolated from Sprague-Dawley rats. Apoptosis rates were assessed by flow cytometry. Ultrastructural characteristics of PMVEC were evaluated by transmission electron microscopy. The protein expression of cleaved caspase-3 was measured using Western blotting. LPS significantly increased the level of apoptosis, induced the appearance of ultrastructural changes typical of apoptosis, up-regulated the expression of active caspase-3 protein. These effects of LPS were attenuated by co-administration of perfluorocarbon. These results suggest that perfluorocarbon can attenuate LPS-induced apoptosis of PMVEC by inhibiting TLR-4 signaling and caspase-3 activation.

摘要

本研究旨在探讨全氟碳化合物对脂多糖诱导的大鼠肺微血管内皮细胞(PMVEC)凋亡的作用及其机制。通过流式细胞术评估细胞凋亡率。透射电镜观察 PMVEC 的超微结构特征。Western blot 法检测裂解型 caspase-3 蛋白的表达。LPS 显著增加细胞凋亡水平,诱导出现典型的凋亡超微结构改变,上调活性 caspase-3 蛋白的表达。全氟碳化合物可减轻 LPS 的这些作用。这些结果表明,全氟碳化合物通过抑制 TLR-4 信号通路和 caspase-3 活化,减轻 LPS 诱导的 PMVEC 凋亡。

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