Here, we investigated the protective efficacy of protocatechuic acid (PCA) against lipopolysaccharide (LPS)-induced septic lung injury. Eighty-two male Balb/c mice were divided into six groups: control, PCA30 (30 mg/kg), LPS (10 mg/kg), PCA10-LPS, PCA20-LPS, and PCA30-LPS treated with 10, 20 and 30 mg/kg PCA, respectively, for seven days before intraperitoneal LPS injection. PCA pre-treatment, especially at higher dose, significantly reduced LPS-induced lung tissue injury as indicated by increased heat shock protein 70 and antioxidant molecules (reduced glutathione, superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) accompanied by lower oxidative stress indices (malondialdehyde and nitric oxide). PCA administration decreased inflammatory mediators including myeloperoxidase, nuclear factor kappa B (NF-κB p65), and pro-inflammatory cytokines, and prevented the development of apoptotic events in the lung tissue. At the molecular level, PCA downregulated mRNA expression of nitric oxide synthase 2, C/EBP homologous protein, and high mobility group box1 in the lungs of all PCA-LPS treated mice. Thus, PCA-pre-treatment effectively counteracted sepsis-induced acute lung injury in vivo by promoting and antioxidant status, while inhibiting inflammation and apoptosis.

中文翻译：

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原儿茶酸减轻脂多糖诱导的小鼠脓毒性肺损伤：通过抑制氧化应激、炎症和细胞凋亡的可能作用

在这里，我们研究了原儿茶酸 (PCA) 对脂多糖 (LPS) 诱导的败血性肺损伤的保护功效。82 只雄性 Balb/c 小鼠分为六组：对照、PCA30（30 毫克/公斤）、LPS（10 毫克/公斤）、PCA10-LPS、PCA20-LPS 和 PCA30-LPS，分别用 10、20 和腹腔内 LPS 注射前 7 天，分别为 30 mg/kg PCA。PCA 预处理，特别是在较高剂量下，显着减少 LPS 诱导的肺组织损伤，如热休克蛋白 70 和抗氧化分子（还原型谷胱甘肽、超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽还原酶）的增加所表明的，伴随着较低的氧化应激指数（丙二醛和一氧化氮）。PCA 给药减少炎症介质，包括髓过氧化物酶、核因子 kappa B (NF-κB p65)、和促炎细胞因子，并阻止肺组织中凋亡事件的发生。在分子水平上，PCA 下调了所有 PCA-LPS 治疗小鼠肺中一氧化氮合酶 2、C/EBP 同源蛋白和高迁移率族 box1 的 mRNA 表达。因此，PCA 预处理通过促进和抗氧化状态在体内有效抵抗败血症诱导的急性肺损伤，同时抑制炎症和细胞凋亡。