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苘麻叶中类黄酮部位通过 NF-κB 和 MAPK 信号通路对脂多糖诱导的急性肺损伤的保护作用。

The protective effect of the flavonoid fraction of Abutilon theophrasti Medic. leaves on LPS-induced acute lung injury in mice via the NF-κB and MAPK signalling pathways.

机构信息

Key Laboratory of Zoonosis of Liaoning Province, College of Animal Science and Veterinary Medicine, Shenyang Agricultural University, No. 120 Dongling Road, Shenhe Dist. 110866, Shenyang Liaoning Prov., People's Republic of China.

Key Laboratory of Zoonosis of Liaoning Province, College of Animal Science and Veterinary Medicine, Shenyang Agricultural University, No. 120 Dongling Road, Shenhe Dist. 110866, Shenyang Liaoning Prov., People's Republic of China.

出版信息

Biomed Pharmacother. 2019 Jan;109:1024-1031. doi: 10.1016/j.biopha.2018.10.197. Epub 2018 Nov 6.

Abstract

Accompanied by the damages of epithelial and capillary endothelial cell, acute lung injury is diagnosed with the typical pathological symptoms in clinic, including diffusing of pulmonary interstitial, alveolar oedema and hypoxic respiratory insufficiency. Current study focused on the investigation the anti-inflammatory action and mechanisms of total flavonoids extract (TFE) from Abutilon theophrasti Medic. leaves on ALI mice induced by LPSs. Mice were administrated intragastrically with TFE at the concentrations of 0.25, 0.5, or 1.0 g/kg for 5 days, and on last day, nasal administration of LPSs for 6 h after 30 min for intragastric administration of TFE. Pretreatment with TFE not only reduced oxidative damage but also alleviated lung edema in ALI mice. Increased secretion of pro-inflammatory cytokines TNF-α, IL-1β and IL-6, caused by LPSs was reversed by TFE; on the contrary, the anti-inflammatory cytokine IL-10 was upregulated. The proteins expressions of pro-inflammatory mediators iNOS and COX-2 induced by LPSs, were down-regulated by TFE. Moreover, the activation of NF-κB and MAPK signalling pathways was inhibited by TFE in LPSs induced ALI mice. The results revealed that the anti-inflammatory mechanisms of TFE were via inhibition of NF-κB and MAPK activation. Combined, the results suggested that TFE might exert in vivo antioxidant and anti-inflammatory functions in LPSs stimulated mice, and will be potential in adjuvant treatment in oxidative stress and inflammation diseases.

摘要

伴随着上皮细胞和毛细血管内皮细胞的损伤,急性肺损伤在临床上以典型的病理症状为诊断依据,包括弥漫性肺间质、肺泡水肿和低氧性呼吸功能不全。本研究重点研究了野靛叶总黄酮提取物(TFE)对脂多糖(LPSs)诱导的急性肺损伤(ALI)小鼠的抗炎作用及其机制。小鼠连续 5 天灌胃给予 TFE,浓度分别为 0.25、0.5 或 1.0 g/kg,最后一天,在灌胃 TFE 30 分钟后,经鼻腔给予 LPSs 6 小时。TFE 预处理不仅减轻了氧化损伤,还减轻了 ALI 小鼠的肺水肿。TFE 逆转了 LPSs 引起的促炎细胞因子 TNF-α、IL-1β 和 IL-6 的过度分泌;相反,抗炎细胞因子 IL-10 被上调。TFE 下调了 LPSs 诱导的 ALI 小鼠中促炎介质 iNOS 和 COX-2 的蛋白表达。此外,TFE 抑制了 LPSs 诱导的 ALI 小鼠中 NF-κB 和 MAPK 信号通路的激活。结果表明,TFE 的抗炎机制是通过抑制 NF-κB 和 MAPK 的激活。综上所述,TFE 可能在 LPS 刺激的小鼠体内发挥抗氧化和抗炎作用,有望成为氧化应激和炎症性疾病的辅助治疗药物。

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