Tang Qi-Feng, Fang Zhi-Yuan, Shi Cheng-Huan
Department of Anesthesiology, Suzhou BenQ Medical Center, Nanjing Medical UniversitySuzhou, Jiangsu Province, China.
Department of Anesthesiology, Suzhou Hospital Affiliated to Nanjing Medical University, Suzhou Municipal HospitalSuzhou, Jiangsu Province, China.
Am J Transl Res. 2017 Apr 15;9(4):1732-1742. eCollection 2017.
Acute lung injury (ALI) is a disturbance caused by infectious or non-infectious inflammation and lipopolysaccharide (LPS) could induce an artificial pathological ALI process. Sevoflurane has been demonstrated to be an inhaled anesthetic having anti-inflammatory and protective effects on inflammatory injury. To study the protective effects and mechanisms of sevoflurane on LPS-induced acute lung injury in mice. By assessing W/D ratio, sevofluranecan counteract the edema induced by LPS. The ELISA results showed that sevoflurane reduced IFN-γ production and increased IL-10 level. Elevation of PGE2 induced by sevofluraneand LPS in peritoneal macrophages was inhibited by NS-398, an inhibitor of the PGE2 regulator COX-2, indicating that NS-398 blocked COX-2 mediated PGE synthesis. NS-398 itself did not cause lung inflammation and mitigated the protective effect of sevoflurane on LPS-induced ALI in mice. LPS changes immune homeostasis, resulting in acute lung inflammatory injury. Inhaled sevoflurane regulates immune homeostasis, thereby playing a protective role in alleviating LPS-induced ALI.
急性肺损伤（ALI）是由感染性或非感染性炎症引起的一种病症，脂多糖（LPS）可诱发人工病理ALI过程。七氟醚已被证明是一种对炎症损伤具有抗炎和保护作用的吸入麻醉剂。为研究七氟醚对LPS诱导的小鼠急性肺损伤的保护作用及机制。通过评估肺湿干重比，七氟醚可对抗LPS诱导的水肿。ELISA结果显示，七氟醚可降低IFN-γ的产生并提高IL-10水平。PGE2调节剂COX-2的抑制剂NS-398可抑制七氟醚和LPS诱导的腹膜巨噬细胞中PGE2的升高，表明NS-398可阻断COX-2介导的PGE合成。NS-398本身不会引起肺部炎症，且会减轻七氟醚对LPS诱导的小鼠ALI的保护作用。LPS改变免疫稳态，导致急性肺部炎症损伤。吸入七氟醚可调节免疫稳态，从而在减轻LPS诱导的ALI中发挥保护作用。
