GPA 肽通过抑制肺泡巨噬细胞的氧化应激和焦亡减轻脓毒症引起的小鼠急性肺损伤,Oxidative Medicine and Cellular Longevity

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GPA 肽通过抑制肺泡巨噬细胞的氧化应激和焦亡减轻脓毒症引起的小鼠急性肺损伤
Oxidative Medicine and Cellular Longevity Pub Date : 2021-12-28 , DOI: 10.1155/2021/5589472
Yukun Liu ₁ , Yongsheng Zhang ₂ , Quanrui Feng ₂ , Qinxin Liu ₂ , Jie Xie ₂ , Hui Li ₂ , Fan Yang ₂ , Xinghua Liu ₂ , Wei Gao ₂ , Xiangjun Bai ₂ , Zhanfei Li ₂ , Yuchang Wang ₂

Affiliation

众所周知，急性肺损伤 (ALI) 是一种破坏性的呼吸道感染形式，并且由于缺乏有效的治疗，是重症监护死亡率的重要原因。炎症、氧化应激和细胞焦亡与多种炎症性疾病如 ALI 相关。人们普遍认为 Gly-Pro-Ala (GPA) 肽在不同种类的炎症性疾病中调节氧化应激和细胞焦亡。我们的研究旨在探索 GPA 肽对 ALI 的调节功能和保护作用。在目前的研究中，盲肠结扎和穿刺（CLP）技术用于诱发小鼠脓毒症，并在 CLP 后以不同浓度（50、100 和 150 mg/kg）腹腔注射 GPA 肽。记录和分析组织病理学变化和肺干湿比。我们还调查了氧化应激、炎症和细胞焦亡的水平。结果表明，GPA 肽显着改善了 CLP 刺激的肺组织损伤，阻碍了促炎细胞因子的释放，并减少了炎症细胞的浸润。此外，GPA 肽抑制肺泡巨噬细胞中的氧化应激和 caspase-1 依赖性细胞焦亡。此外，我们的研究表明，GPA 肽通过减弱 ROS 来防止肺泡巨噬细胞发生焦亡。总之，结果表明，GPA 肽通过抑制氧化应激以及肺泡巨噬细胞的焦亡对 CLP 刺激的 ALI 具有保护作用。结果表明，GPA 肽显着改善了 CLP 刺激的肺组织损伤，阻碍了促炎细胞因子的释放，并减少了炎症细胞的浸润。此外，GPA 肽抑制肺泡巨噬细胞中的氧化应激和 caspase-1 依赖性细胞焦亡。此外，我们的研究表明，GPA 肽通过减弱 ROS 来防止肺泡巨噬细胞发生焦亡。总之，结果表明，GPA 肽通过抑制氧化应激以及肺泡巨噬细胞的焦亡对 CLP 刺激的 ALI 具有保护作用。结果表明，GPA 肽显着改善了 CLP 刺激的肺组织损伤，阻碍了促炎细胞因子的释放，并减少了炎症细胞的浸润。此外，GPA 肽抑制肺泡巨噬细胞中的氧化应激和 caspase-1 依赖性细胞焦亡。此外，我们的研究表明，GPA 肽通过减弱 ROS 来防止肺泡巨噬细胞发生焦亡。总之，结果表明，GPA 肽通过抑制氧化应激以及肺泡巨噬细胞的焦亡对 CLP 刺激的 ALI 具有保护作用。GPA 肽抑制肺泡巨噬细胞中的氧化应激和 caspase-1 依赖性细胞焦亡。此外，我们的研究表明，GPA 肽通过减弱 ROS 来防止肺泡巨噬细胞发生焦亡。总之，结果表明，GPA 肽通过抑制氧化应激以及肺泡巨噬细胞的焦亡对 CLP 刺激的 ALI 具有保护作用。GPA 肽抑制肺泡巨噬细胞中的氧化应激和 caspase-1 依赖性细胞焦亡。此外，我们的研究表明，GPA 肽通过减弱 ROS 来防止肺泡巨噬细胞发生焦亡。总之，结果表明，GPA 肽通过抑制氧化应激以及肺泡巨噬细胞的焦亡对 CLP 刺激的 ALI 具有保护作用。

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GPA Peptide Attenuates Sepsis-Induced Acute Lung Injury in Mice via Inhibiting Oxidative Stress and Pyroptosis of Alveolar Macrophage

Acute lung injury (ALI) has been known to be a devastating form of respiratory infection and an important contributor to mortality in intensive care, due to its lacking of effective treatment. Inflammation, oxidative stress, and pyroptosis are associated with multiple kinds of inflammatory diseases such as ALI. It is commonly accepted that Gly-Pro-Ala (GPA) peptide regulates oxidative stress and pyroptosis in different kinds of inflammatory diseases. Our study is aimed at exploring the regulatory function and protective effects of GPA peptides on ALI. In the current study, the cecal ligation and puncture (CLP) technique was used to evoke sepsis in mice, and GPA peptide was administered intraperitoneally with different concentrations (50, 100, and 150 mg/kg) after CLP. Histopathological changes and the ratio of wet-to-dry in lung were recorded and analyzed. We also investigated the level of oxidative stress, inflammation, and pyroptosis. Results showed that GPA peptide significantly ameliorated CLP-stimulated lung tissue injury, impeded proinflammatory cytokine release, and reduced inflammatory cell infiltration. Additionally, GPA peptide suppressed oxidative stress and caspase-1-dependent pyroptosis in alveolar macrophages. Furthermore, our study showed that the GPA peptide prevents alveolar macrophage from undergoing pyroptosis by attenuating ROS. In conclusion, results demonstrated that GPA peptide has protective effects in CLP-stimulated ALI by inhibiting oxidative stress as well as pyroptosis of alveolar macrophage.

更新日期：2021-12-28

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