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首页> 外文期刊>RSC Advances >Umbelliferone attenuates lipopolysaccharide-induced acute lung injury linked with regulation of TLRs-MyD88 and RIP140/NF-kappa B signaling pathways
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Umbelliferone attenuates lipopolysaccharide-induced acute lung injury linked with regulation of TLRs-MyD88 and RIP140/NF-kappa B signaling pathways

机译：伞形酮减轻脂多糖诱导的急性肺损伤，与TLRs-MyD88和RIP140 /NF-κB信号通路的调节有关

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摘要

Umbelliferone (Umb), isolated from the chloroform fraction of Potentilla evestita, exerts a variety of pharmacological activities. The aim of the present study was to evaluate the protective effects and possible mechanisms of Umb on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Male BALB/c mice were randomly divided into five groups: control group, LPS group, LPS + dexamethasone (Dex, 2 mg kg(-1)) group, LPS + Umb (20 mg kg(-1)) group, and LPS + Umb (Umb, 40 mg kg(-1)) group. Umb and Dex were orally administered 15 min before the intra-tracheal (IT) administration of LPS. 6 h later, the mice were sacrificed. The lung tissues and bronchoalveolar fluid (BALF) were prepared for further analysis. Our results showed that pretreatment with Umb prior to the LPS challenge significantly decreased the lung W/D weight ratio, total leukocyte number and neutrophil percentage in the BALF. Umb also reduced pulmonary MPO activity and alleviated histopathological alteration. Besides, the contents of inflammatory cytokines including interleukin (IL)-6, interleukin (IL)-1 beta and tumor neurosis factor (TNF)-alpha were also found to be significantly inhibited by Umb in BALF. Furthermore, the expressions of TLR2, TLR4, MyD88, receptor-interacting protein 140 (RIP140), RelA, CBP, nuclear factor kappa B (NF-kappa B), caspase-9, caspase-3, Bax in lung tissues were inhibited and Bcl-2 expression was increased in the LPS + Umb group. These results showed that administration of Umb could attenuate LPS-induced ALI, possibly via the anti-inflammatory and anti-apoptotic activities through the TLRs-MyD88 and RIP140/NF-kappa B pathway.
机译：从委陵菜委陵菜的氯仿馏分中分离出的伞形酮（Umb）具有多种药理活性。本研究的目的是评估Umb对脂多糖（LPS）诱导的小鼠急性肺损伤（ALI）的保护作用和可能的机制。将雄性BALB / c小鼠随机分为5组：对照组，LPS组，LPS +地塞米松（Dex，2 mg kg（-1））组，LPS + Umb（20 mg kg（-1））组和LPS + Umb（Umb，40 mg kg（-1））组。在气管内（LP）气管内（IT）给药前15分钟口服Umb和Dex。 6小时后，处死小鼠。准备肺组织和支气管肺泡液（BALF）进行进一步分析。我们的结果表明，在LPS攻击之前用Umb进行预处理可显着降低BALF中的肺W / D重量比，总白细胞数和中性粒细胞百分比。 Umb还降低了肺MPO活性并减轻了组织病理学改变。此外，BALF中的Umb还发现白细胞介素（IL）-6，白介素（IL）-1β和肿瘤神经症因子（TNF）-α等炎性细胞因子的含量受到显着抑制。此外，肺组织中TLR2，TLR4，MyD88，受体相互作用蛋白140（RIP140），RelA，CBP，核因子κB（NF-κB），caspase-9，caspase-3，Bax的表达被抑制并在LPS + Umb组中，Bcl-2表达增加。这些结果表明，Umb的施用可能通过TLRs-MyD88和RIP140 /NF-κB途径的抗炎和抗凋亡活性而减弱LPS诱导的ALI。

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