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脂蛋白不会调节脂多糖刺激人单核细胞所诱导的组织因子活性、纤溶酶原激活物或肿瘤坏死因子的产生。

Lipoproteins do not modulate the tissue factor activity, plasminogen activator or tumour necrosis factor production induced by lipopolysaccharide stimulation of human monocytes.

作者信息

Schlichting E, Henriksen T, Lyberg T

机构信息

Department of Surgery, Ullevål University Hospital, Oslo, Norway.

出版信息

Scand J Clin Lab Invest. 1994 Oct;54(6):465-73. doi: 10.3109/00365519409085471.

Abstract

Upon stimulation with lipopolysaccharides (LPS), monocytes are able to produce tissue factor (TF), the most powerful physiological procoagulant substance known. In several assay systems LPS bound to lipoprotein has been reported to be less active than unbound LPS in stimulating monocytes. In the present study the LPS-induced TF activity was, however, not prevented by lipoproteins (VLDL, LDL, HDL). In fact, the very low density (VLDL) fraction further increased the TF inducing capacity of LPS. The lipoproteins per se mediated reduced plasminogen activator (PA) production in monocytes. LPS had an even more and significant depressing effect on PA production, which was not further decreased in the presence of lipoproteins. Furthermore, LPS-induced release of tumour necrosis factor (TNF), a marker of monocyte activity, was not inhibited by lipoproteins. Our experiments suggest that lipoproteins do not render LPS less effective in stimulating TNF release, procoagulant and fibrinolytic activities in human monocytes.

摘要

在用脂多糖(LPS)刺激时,单核细胞能够产生组织因子(TF),这是已知最强有力的生理性促凝物质。在多个检测系统中,据报道与脂蛋白结合的LPS在刺激单核细胞方面的活性低于未结合的LPS。然而,在本研究中,脂蛋白(极低密度脂蛋白、低密度脂蛋白、高密度脂蛋白)并未阻止LPS诱导的TF活性。事实上,极低密度(VLDL)部分进一步增强了LPS诱导TF的能力。脂蛋白本身介导单核细胞中纤溶酶原激活物(PA)生成减少。LPS对PA生成有更强且显著的抑制作用,在存在脂蛋白的情况下PA生成并未进一步减少。此外,LPS诱导的肿瘤坏死因子(TNF)释放,即单核细胞活性的一个标志物,未被脂蛋白抑制。我们的实验表明,脂蛋白不会使LPS在刺激人单核细胞的TNF释放、促凝和纤溶活性方面效果降低。

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