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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Pentosan polysulfate protects brain endothelial cells against bacterial lipopolysaccharide-induced damages.
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Pentosan polysulfate protects brain endothelial cells against bacterial lipopolysaccharide-induced damages.

机译：戊聚糖多硫酸盐可保护脑内皮细胞免受细菌脂多糖诱导的损害。

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摘要

Peripheral inflammation can aggravate local brain inflammation and neuronal death. The blood-brain barrier (BBB) is a key player in the event. On a relevant in vitro model of primary rat brain endothelial cells co-cultured with primary rat astroglia cells lipopolysaccharide (LPS)-induced changes in several BBB functions have been investigated. LPS-treatment resulted in a dose- and time-dependent decrease in the integrity of endothelial monolayers: transendothelial electrical resistance dropped, while flux of permeability markers fluorescein and albumin significantly increased. Immunostaining for junctional proteins ZO-1, claudin-5 and beta-catenin was significantly weaker in LPS-treated endothelial cells than in control monolayers. LPS also reduced the intensity and changed the pattern of ZO-1 immunostaining in freshly isolated rat brain microvessels. The activity of P-glycoprotein, an important efflux pump at the BBB, was also inhibited by LPS. At the same time production of reactive oxygen species and nitric oxide was increased in brain endothelial cells treated with LPS. Pentosan polysulfate, a polyanionic polysaccharide could reduce the deleterious effects of LPS on BBB permeability, and P-glycoprotein activity. LPS-stimulated increase in the production of reactive oxygen species and nitric oxide was also decreased by pentosan treatment. The protective effect of pentosan for brain endothelium can be of therapeutical significance in bacterial infections affecting the BBB.
机译：周围炎症可加剧局部脑部炎症和神经元死亡。血脑屏障（BBB）是事件的关键参与者。在与原代大鼠星形胶质细胞共培养的原代大鼠脑内皮细胞的相关体外模型中，研究了脂多糖（LPS）诱导的几种血脑屏障功能变化。 LPS处理导致内皮单层完整性的剂量和时间依赖性降低：内皮电阻降低，而通透性标志物荧光素和白蛋白的通量显着增加。连接蛋白ZO-1，claudin-5和β-catenin的免疫染色在LPS处理的内皮细胞中明显弱于对照单层细胞。 LPS还降低了强度，并改变了新鲜分离的大鼠脑微血管中ZO-1免疫染色的模式。 LPS也抑制了P-糖蛋白（BBB上的重要外排泵）的活性。同时，LPS处理的脑内皮细胞中活性氧和一氧化氮的产生增加。戊聚糖多硫酸盐（一种多聚阴离子多糖）可以减少LPS对BBB渗透性和P-糖蛋白活性的有害作用。 LPS刺激的戊聚糖处理还可以减少活性氧和一氧化氮的产生。戊聚糖对脑内皮的保护作用在影响BBB的细菌感染中具有治疗意义。

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