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牡荆素通过抑制 NF-κB 和 NLRP3 信号通路改善脂多糖诱导的小鼠急性肺损伤。

Fraxin ameliorates lipopolysaccharide-induced acute lung injury in mice by inhibiting the NF-κB and NLRP3 signalling pathways.

机构信息

School of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, PR China; Key Laboratory of Material Basis Analysis of Chinese Medicine, Shaanxi Administration of Traditional Chinese Medicine, Xi'an 710061, PR China.

School of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, PR China; Key Laboratory of Material Basis Analysis of Chinese Medicine, Shaanxi Administration of Traditional Chinese Medicine, Xi'an 710061, PR China.

出版信息

Int Immunopharmacol. 2019 Feb;67:1-12. doi: 10.1016/j.intimp.2018.12.003. Epub 2018 Dec 6.

DOI:10.1016/j.intimp.2018.12.003
PMID:30530164
Abstract

Fraxin, the effective component of the Chinese traditional medicine Cortex Fraxini, is reported to have anti-inflammatory effects. This study assessed the anti-inflammatory effect of fraxin on the lipopolysaccharide (LPS)-induced inflammatory response in A549 cells and the protective efficacy on LPS-induced acute lung injury (ALI) in mice. Fraxin reduced LPS-induced TNF-α, IL-6 and IL-1β production in A549 cells and alleviated the LPS-induced wet/dry (W/D) weight ratio and the effects observed via histopathological examination of the lung in vivo. Furthermore, fraxin reduced the protein concentrations in the broncho-alveolar lavage (BAL) fluid and cytokine production in the sera. Fraxin also clearly attenuated the oxidation index, including the activity of myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH). Immunohistochemistry analysis showed that fraxin suppressed LPS-induced inflammatory damage. The expression of proteins involved in the NF-κB and NLRP3 inflammatory corpuscle signalling pathways was consistent between the lung tissues and cell samples. Overall, fraxin played a protective role in LPS-induced lung injury by inhibiting the NF-κB and NLRP3 signalling pathways.

摘要

秦皮是中药秦皮的有效成分,具有抗炎作用。本研究评估了秦皮对脂多糖(LPS)诱导的 A549 细胞炎症反应的抗炎作用,以及对 LPS 诱导的急性肺损伤(ALI)的保护作用。秦皮降低了 LPS 诱导的 A549 细胞中 TNF-α、IL-6 和 IL-1β的产生,并减轻了 LPS 诱导的体内肺湿/干(W/D)重量比和组织病理学检查的影响。此外,秦皮降低了支气管肺泡灌洗液(BAL)中蛋白浓度和血清中细胞因子的产生。秦皮还明显减弱了氧化指标,包括髓过氧化物酶(MPO)、丙二醛(MDA)、超氧化物歧化酶(SOD)和谷胱甘肽(GSH)的活性。免疫组化分析表明,秦皮抑制了 LPS 诱导的炎症损伤。肺组织和细胞样本中与 NF-κB 和 NLRP3 炎症小体信号通路相关的蛋白表达一致。总的来说,秦皮通过抑制 NF-κB 和 NLRP3 信号通路在 LPS 诱导的肺损伤中发挥保护作用。

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