The protective effect and mechanism of sevoflurane on LPS-induced acute lung injury in mice

• Published in: American journal of translational research Vol. 9; no. 4; pp. 1732 - 1742
• Main Authors: Tang, Qi-Feng, Fang, Zhi-Yuan, Shi, Cheng-Huan
• Format: Journal Article
• Language: English
• Published: United States e-Century Publishing Corporation 01.01.2017
• Subjects: Original; Sevoflurane; PGE2; IFN-γ; acute lung injury; IL-10
• ISSN: 1943-8141; 1943-8141

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.