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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >LPS-RS attenuation of lipopolysaccharide-induced acute lung injury involves NF-kappa B inhibition
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LPS-RS attenuation of lipopolysaccharide-induced acute lung injury involves NF-kappa B inhibition

机译：LPS-RS减轻脂多糖诱导的急性肺损伤涉及NF-κB抑制

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In this study, we studied the effect of lipopolysaccharide from Rhodobacter sphaeroides (LPS-RS), an inhibitor of Toll-like receptor 4 (TLR4), in LPS-induced acute lung injury (ALI). Male Sprague-Dawley rats were treated with LPS-RS (0.1 mg/kg body mass, by intraperitoneal (i.p.) injection) 1 h before LPS injection (10 mg/kg, i.p.). Bronchoalveolar lavage fluid (BALF) and lung tissues were collected 24 h later to determine total and differential cell count, total protein content, levels of lactate dehydrogenase (LDH), histopathological changes, markers of oxidative stress, and mRNA expression of the inhibitory protein nuclear factor kappaB-alpha (NF kappa BIA) and TLR4. Additionally, rings of pulmonary artery were isolated for measuring vascular reactivity. LPS-induced ALI was indicated by increases in total and differential cell count, total protein, and LDH in BALF, and increased lung levels of malondialdehyde (MDA), as well as decreased activity of reduced glutathione (GSH) and superoxide dismutase (SOD). Moreover, LPS increased pulmonary artery contraction in response to phenylephrine (PE). Additionally, LPS downregulated mRNA expression of NF kappa BIA and upregulated mRNA expression of TLR4. LPS caused a marked inflammation in the lung tissue, with tubercular granuloma and numerous neutrophils. Pretreatment with LPS-RS protected against LPS-induced ALI by decreasing total and differential cell count, total protein, and LDH in BALF, and increased pulmonary GSH content and SOD activity without affecting MDA content. Additionally, it decreased the elevated PE-induced pulmonary artery contraction. LPS-RS upregulated mRNA expression of NF kappa BIA and downregulated mRNA expression of TLR4. Moreover, LPS-RS prevented inflammation in lung tissues. In conclusion, pretreatment with LPS-RS protects against LPS-induced ALI in rats through its anti-inflammatory effects, possibly by decreasing the mRNA expression of TLR4 and increasing that of NF kappa BIA.
机译：在这项研究中，我们研究了脂多糖红球菌（LPS-RS）（一种Toll样受体4（TLR4）的抑制剂）在LPS诱导的急性肺损伤（ALI）中的作用。在LPS注射（10 mg / kg，i.p.）前1小时，以LPS-RS（0.1 mg / kg体重，通过腹膜内（i.p.）注射）处理雄性Sprague-Dawley大鼠。 24小时后收集支气管肺泡灌洗液（BALF）和肺组织，以确定总和差异细胞计数，总蛋白含量，乳酸脱氢酶（LDH）水平，组织病理学变化，氧化应激标志物和抑制性蛋白核的mRNA表达因子κB-α（NFκBIA）和TLR4。另外，分离肺动脉环以测量血管反应性。 LPS诱导的ALI表现为BALF中总细胞数和差异细胞数，总蛋白质和LDH增加，肺中丙二醛（MDA）水平升高，还原型谷胱甘肽（GSH）和超氧化物歧化酶（SOD）活性降低。此外，LPS增加了对苯肾上腺素（PE）的肺动脉收缩。此外，LPS下调NFκBIA的mRNA表达，并上调TLR4的mRNA表达。 LPS在肺组织，结核性肉芽肿和大量中性粒细胞中引起明显的炎症。用LPS-RS进行的预处理可通过减少BALF中的总细胞数和差异细胞数，总蛋白质和LDH来抵抗LPS诱导的ALI，并增加肺GSH含量和SOD活性，而不影响MDA含量。另外，它减少了PE引起的肺动脉收缩的升高。 LPS-RS上调NFκBIA的mRNA表达，下调TLR4的mRNA表达。而且，LPS-RS预防了肺组织的炎症。总之，用LPS-RS进行预处理可通过其抗炎作用保护LPS诱导的大鼠ALI，可能是通过降低TLR4的mRNA表达并增加NFκBIA的表达。

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