Department of Thoracic and Cardiovascular Surgery, Huangshi Central Hospital (Affiliated Hospital of Hubei Polytechnic University), Edong Healthcare Group, Huangshi, Hubei, China.
Free Radic Res. 2021 Jan;55(1):1-10. doi: 10.1080/10715762.2020.1852234. Epub 2020 Dec 1.
Inflammation and oxidative stress contribute to the initiation and progression of septic lung injury. MicroRNA-217 () is proved to be involved in controlling inflammatory response and oxidative stress, yet its role and underlying mechanism in the pathogenesis of septic lung injury remain elusive. Caecal ligation and puncture surgery were performed to generate sepsis and mice were kept for 12 h to imitate septic lung injury. Next, mice were administrated with antagomir or agomir to decrease or increase the expression of in lung tissue. Moreover, primary peritoneal macrophages were separated and incubated with lipopolysaccharide (LPS) to further verify the role of . was upregulated in septic lungs and primary macrophages. antagomir alleviated, whereas agomir aggravated inflammation and oxidative stress in septic mice and LPS-stimulated macrophages. Further detection identified SIRT1 was responsible for antagomir-mediated anti-inflammatory and anti-oxidant effects, and SIRT1 inhibition abolished the beneficial effects of antagomir and . Our data defined as a therapeutic target for treating septic lung injury.
炎症和氧化应激导致脓毒症肺损伤的发生和进展。微小 RNA-217 () 被证明参与调控炎症反应和氧化应激，但其在脓毒症肺损伤发病机制中的作用和潜在机制仍不清楚。通过盲肠结扎和穿刺手术来制造脓毒症模型，并使小鼠持续 12 小时以模拟脓毒症肺损伤。接着，给小鼠施用 反义寡核苷酸或激动剂来降低或增加肺组织中 的表达。此外，分离原代腹腔巨噬细胞并与脂多糖 (LPS) 孵育，以进一步验证 的作用。在脓毒症肺和原代巨噬细胞中，上调。反义寡核苷酸减轻，而激动剂加重脓毒症小鼠和 LPS 刺激的巨噬细胞中的炎症和氧化应激。进一步的检测表明 SIRT1 负责 反义寡核苷酸介导的抗炎和抗氧化作用，而 SIRT1 抑制消除了 反义寡核苷酸和 的有益作用。我们的数据将 定义为治疗脓毒症肺损伤的治疗靶点。
