Pneumonia is a kind of inflammatory disease characterized by pathogen infection of lower respiratory track. Lipopolysaccharide (LPS) is the main bioactive component of Gram-negative bacteria responsible for inflammatory response. Recently, coniferyl aldehyde (CA) has been reported to play a crucial role because of its anti-inflammatory activity. However, the effect and mechanisms of CA in ameliorating symptoms of acute pneumonia remain unknown. Evaluating and identifying the value and exploring the mechanisms of CA on LPS-mediated WI-38 apoptosis and inflammation were the aims of this study. Here, CCK-8 cell viability assay was applied on WI-38 after treatment with or without LPS at different doses of CA to verify that CA can increase LPS-induced cell viability. Then, quantitative polymerase chain reaction (qPCR) and enzyme-linked-immunosorbent serologic assays (ELISA) suggested that LPS treatment dramatically decreased the expression level of IL-10 (anti-inflammatory factor) while strikingly increasing the expression levels of IL-1β, IL-6, and TNF-α (tumor necrosis factor-α; proinflammatory factor) whereas CA treatment attenuates LPS-induced inflammation of WI-38. Further, flow cytometry and Western blot assay verified that LPS treatment dramatically promoted apoptosis of WI-38 cells, while administration of CA notably inhibited apoptosis of WI-38 cells. Moreover, the Western blot assay hinted that CA could inactivate LPS-induced JAK2-STAT1 signaling pathway. These findings indicated that CA could alleviate LPS-mediated WI-38 apoptosis and inflammation injury through JAK2-STAT1 pathway in acute pneumonia.

中文翻译：

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松柏醛通过 JAK2-STAT1 通路在急性肺炎中减轻 LPS 诱导的 WI-38 细胞凋亡和炎症损伤。

肺炎是一种以病原体感染下呼吸道为特征的炎症性疾病。脂多糖 (LPS) 是革兰氏阴性菌的主要生物活性成分，负责炎症反应。最近，据报道松柏醛（CA）因其抗炎活性而发挥关键作用。然而，CA在改善急性肺炎症状方面的作用和机制仍然未知。本研究旨在评估和鉴定CA对LPS介导的WI-38细胞凋亡和炎症的价值和机制。在这里，在用或不用 LPS 以不同剂量的 CA 处理后，在 WI-38 上应用 CCK-8 细胞活力测定，以验证 CA 可以增加 LPS 诱导的细胞活力。然后，定量聚合酶链反应 (qPCR) 和酶联免疫吸附血清测定 (ELISA) 表明 LPS 治疗显着降低了 IL-10（抗炎因子）的表达水平，同时显着增加了 IL-1β、IL- 6，和 TNF-α（肿瘤坏死因子-α；促炎因子），而 CA 治疗减弱 LPS 诱导的 WI-38 炎症。此外，流式细胞术和蛋白质印迹分析证实，LPS 处理显着促进了 WI-38 细胞的凋亡，而 CA 显着抑制了 WI-38 细胞的凋亡。此外，Western印迹分析提示CA可以使LPS诱导的JAK2-STAT1信号通路失活。这些发现表明CA可以通过JAK2-STAT1通路减轻LPS介导的WI-38细胞凋亡和炎症损伤急性肺炎。