Oxidative stress and inflammatory responses are nearly involved in the pathogenesis of various diseases, including acute lung injury (ALI). Orientin (Ori), a flavonoid component extracted from natural plants, displayed anti-inflammatory and antioxidant properties in our previous studies. In the current study, we aimed to investigate the amelioration effect of Ori on lipopolysaccharide (LPS)-induced ALI, and we further explored the potential molecular mechanisms. The present results indicated that Ori effectively alleviated LPS-induced ALI by improving the histological changes of lung; decreasing the lung W/D ratio and protein levels, the release of inflammatory cells and cytokines into the bronchoalveolar lavage fluid (BALF); inhibiting nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and high mobility group box 1 (HMGB1) protein expression; reducing malondialdehyde (MDA) formation and reactive oxygen species (ROS) generation; and increasing the content of glutathione (GSH) and superoxide dismutase (SOD) contents. Moreover, Ori treatment not only significantly suppressed the LPS-induced nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP3) inflammasome, and nuclear factor-kappa B (NF-κB) signaling pathway activation, but also obviously restored the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), NAD (P) H: quinone oxidoreductase (NQO1), glutamate-cysteine ligase catalytic (GCLC), and heme oxygenase 1 (HO-1) expression in the lung; all of which are reduced by LPS. Taken together, these data suggested that Ori plays an important role in the protection against ALI by suppressing inflammation and oxidative stress which may be strongly related to the suppression of NLRP3 inflammasome and NF-κB activation, as well as the upregulation of the Nrf2 signaling pathway.

氧化应激和炎症反应几乎参与多种疾病的发病机制，包括急性肺损伤（ALI）。 Orientin (Ori) 是一种从天然植物中提取的黄酮类成分，在我们之前的研究中显示出抗炎和抗氧化特性。在本研究中，我们旨在研究O​​ri对脂多糖（LPS）诱导的ALI的改善作用，并进一步探讨其潜在的分子机制。目前的结果表明，Ori 通过改善肺的组织学变化，有效缓解 LPS 诱导的 ALI；降低肺W/D比和蛋白质水平，炎症细胞和细胞因子释放到支气管肺泡灌洗液（BALF）中；抑制一氧化氮合酶 (iNOS)、环氧合酶-2 (COX-2) 和高迁移率族蛋白 1 (HMGB1) 蛋白表达；减少丙二醛（MDA）的形成和活性氧（ROS）的产生；并增加谷胱甘肽（GSH）和超氧化物歧化酶（SOD）的含量。此外，Ori治疗不仅显着抑制LPS诱导的核苷酸结合域（NOD）样受体蛋白3（NLRP3）炎症小体和核因子-κB（NF-κB）信号通路的激活，而且还明显恢复表达肺中核因子红细胞 2 相关因子 2 (Nrf2)、NAD (P) H：醌氧化还原酶 (NQO1)、谷氨酸半胱氨酸连接酶催化 (GCLC) 和血红素加氧酶 1 (HO-1) 的表达；所有这些都被 LPS 减少。 综上所述，这些数据表明 Ori 通过抑制炎症和氧化应激在预防 ALI 中发挥重要作用，这可能与抑制 NLRP3 炎性体和 NF-κB 激活以及上调 Nrf2 信号通路密切相关。 。