Lonicera japonica Thunb (LJT) is a commonly used herbal soup to treat inflammation-related diseases. However, the effect of LJT on ALI is unknown. The present study was aimed at investigating the protective effects of LJT extract (LTE) and its active ingredient luteolin (Lut) on lipopolysaccharide (LPS)-stimulated ALI and investigate its potential mechanism. The effects of LTE and Lut were explored in an ALI mouse model induced by intraperitoneal injection of lipopolysaccharide (LPS). Besides, the LPS-induced inflammation model in BEAS-2B cells was used to clarify the underlying mechanisms. The ALI pathological changes in lung tissues were tested through Haematoxylin and eosin (HE) staining. The apoptosis of cells in lung tissue and the cell model in vitro was evaluated by TUNEL assays, respectively. Meanwhile, the viability of cells in vitro was evaluated by Cell Counting Kit-8 (CCK-8) assay. The levels/concentrations of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1β and IL-10 in BALF were detected by enzyme-linked immunosorbent assay (ELISA). Besides, through quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting, the expression of the above-mentioned inflammatory factors and key factors in the NF-κB signaling pathway was examined. The distribution of inflammatory factors in tissue was observed through immunohistochemistry (IHC) assays . In relative to LPS-stimulated group, the in vivo study showed that LTE and different concentrations of Lut dramatically alleviated LPS-evoked lung pathological injury and lung edema based on the changes in total protein levels and lung wet/dry (W/D) ratio in the bronchoalveolar lavage fluid (BALF) from ALI mice. LTE and different concentrations of Lut also suppressed the inflammatory response, as reflected by the variations of neutrophil accumulation and the production of proinflammatory and anti-inflammatory cytokines in the lung tissues and BALF of ALI mice. The in vitro research also demonstrated that LTE and Lut visibly facilitated cell viability and restrained the apoptosis of BEAS-2B cells stimulated by LPS. Lut hindered LPS-inducible activation of NF-κB pathway in BEAS-2B cells. The present study proved that LTE might suppress LPS-induced acute injury and inflammation in mice and BEAS-2B cells through the Lut-caused suppression of NF-κB signal path (Figure 1).

中文翻译：

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金银花提取物可改善脂多糖诱导的急性肺损伤，该损伤与木犀草素介导的 NF-κB 信号通路抑制相关

Lonicera japonica Thunb (LJT) 是一种常用的草药汤，用于治疗炎症相关疾病。然而，LJT 对 ALI 的作用尚不清楚。本研究旨在探讨 LJT 提取物 (LTE) 及其活性成分木犀草素 (Lut) 对脂多糖 (LPS) 刺激的 ALI 的保护作用并探讨其潜在机制。在腹腔注射脂多糖（LPS）诱导的 ALI 小鼠模型中探讨了 LTE 和 Lut 的作用。此外，BEAS-2B细胞中LPS诱导的炎症模型被用来阐明潜在的机制。通过苏木精和伊红（HE）染色检测肺组织的ALI病理变化。分别采用TUNEL法评价肺组织和体外细胞模型中细胞的凋亡情况。同时，通过细胞计数试剂盒-8（CCK-8）测定评估细胞的体外活力。采用酶联免疫吸附法（ELISA）检测BALF中肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、IL-1β和IL-10的水平/浓度。此外，通过实时定量聚合酶链反应（qRT-PCR）和Western blotting检测上述炎症因子和NF-κB信号通路关键因子的表达情况。通过免疫组织化学（IHC）检测观察组织中炎症因子的分布。相对于LPS刺激组，体内研究表明，基于总蛋白水平和肺湿/干（W/D）比的变化，LTE和不同浓度的Lut显着减轻了LPS引起的肺病理损伤和肺水肿ALI 小鼠的支气管肺泡灌洗液 (BALF) 中。 LTE 和不同浓度的 Lut 还抑制了炎症反应，这可以从 ALI 小鼠肺组织和 BALF 中中性粒细胞积累以及促炎和抗炎细胞因子产生的变化反映出来。体外研究还表明，LTE 和 Lut 明显促进细胞活力并抑制 LPS 刺激的 BEAS-2B 细胞凋亡。 Lut 阻碍 BEAS-2B 细胞中 LPS 诱导的 NF-κB 通路激活。本研究证明，LTE 可能通过 Lut 引起的 NF-κB 信号通路抑制来抑制 LPS 诱导的小鼠和 BEAS-2B 细胞的急性损伤和炎症（图 1）。