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Exogenous surfactant suppresses inflammation in experimental endotoxin-induced lung injury.

机译:外源性表面活性剂抑制实验性内毒素诱导的肺损伤中的炎症。

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摘要

Our objective was to evaluate the anti-inflammatory effects of exogenous surfactant and surfactant phospholipids on the lipopolysaccharide (LPS)-induced lung injury. Exogenous surfactant (porcine surfactant) and surfactant phospholipid (dipalmitoyl phospholipid DPPC, hexadecanol, tylaxopol) were instilled intratracheally with LPS in rats. Expression of surfactant apoproteins (SP-A) and the cyclooxygenase enzymes (COX-1 and -2) was studied by immunohistochemistry, and apoptosis was analyzed by in situ terminal dUTP nick end labeling TUNEL assay. The intracellular reactive oxygen species (ROS) was measured in the isolated macrophages by fluorescence measurement with dichlorofluorescein diacetate (DCFH-DA). LPS-induced oxidative burst and apoptosis at 72 hours were reduced by both porcine and synthetic surfactant. SP-A as well as COX-1 and -2 expressions were suppressed with synthetic surfactant treatment, whereas with porcine surfactant (P-SF) the SP-A expression was enhanced in response to LPS administration. These results indicate that exogenous surfactant inhibits LPS-induced inflammation. This anti-inflammatory activity may be an important outcome of surfactant therapy in endotoxin-induced respiratory distress.
机译:我们的目标是评估外源性表面活性剂和表面活性剂磷脂对脂多糖(LPS)诱导的肺损伤的抗炎作用。在大鼠中,气管内滴注了外源性表面活性剂(猪表面活性剂)和表面活性剂磷脂(二棕榈酰磷脂DPPC,十六烷醇,tylaxopol)。通过免疫组织化学研究表面活性剂载脂蛋白(SP-A)和环氧合酶(COX-1和-2)的表达,并通过原位末端dUTP缺口末端标记TUNEL法分析细胞凋亡。通过用二氯荧光素二乙酸酯(DCFH-DA)进行荧光测量,在分离的巨噬细胞中测量细胞内活性氧(ROS)。猪和合成表面活性剂均可减少LPS诱导的72小时氧化爆发和细胞凋亡。合成表面活性剂处理可抑制SP-A以及COX-1和-2的表达,而猪表面活性剂(P-SF)响应于LPS给药可提高SP-A的表达。这些结果表明外源性表面活性剂抑制LPS诱导的炎症。这种抗炎活性可能是表面活性剂治疗内毒素引起的呼吸窘迫的重要结果。

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