Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Sevoflurane improves gaseous exchange and exerts protective effects in lipopolysaccharide-induced lung injury in mice models

Wei-Min Shen¹, Che Li², Yan-Hua Yuan³, Ying-Xue Xu⁴, Yong-Liang Chi⁴

¹Department of Pharmacy; ²Department of Spine Surgery; ³Department of Well-known Specialist, Shandong Provincial Hospital; ⁴Department of Anesthesiology, The Affiliated Hospital of Shandong Traditional Chinese Medicine University, Jinan City 250014, Shandong Province, China.

For correspondence:- Yong-Liang Chi Email: ADossibehe@yahoo.com Tel:+8653168617021

Accepted: 5 October 2017 Published: 31 January 2018

Citation: Shen W, Li C, Yuan Y, Xu Y, Chi Y. Sevoflurane improves gaseous exchange and exerts protective effects in lipopolysaccharide-induced lung injury in mice models. Trop J Pharm Res 2018; 17(1):47-52 doi: 10.4314/tjpr.v17i1.8

© 2018 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the protective effect of sevoflurane against lipopolysaccharide (LPS)-induced acute liver injury (ALI) in amice model.

Methods: Seven week-old female BalB/C mice were used. Lung water content and cell count were estimated by standard protocols. Cytokine and chemokine analysis was performed using commercially available kits. Myeloperoxidase activity was evaluated spectrophotometrically while histopathological analysis was carried out by H and E staining.

Results: The results revealed that sevoflurane treatment significantly improved gaseous exchange, and reduced lung water content and lung inflammation as evidenced by a decrease in neutrophil migration into BALF (p < 0.01). Sevoflurane also significantly reversed the LPS-triggered suppression of IL-10 in the lung tissues of LPS-treated mice, when compared to saline-treated controls (p < 0.01). It reversed LPS-induced oxidative stress, as demonstrated by increase in total antioxidant capacity (T-AC), catalase (CAT) and superoxide dismutase-1 (SOD-1), as well as an increase in reduced/oxidized glutathione (GSH/GSSG) ratio. In addition, sevoflurane blocked LPS-induced lung tissue injury in ALI mice, and exerted protective effects against acute LPS-induced lung injury.

Conclusion: These results suggest that sevoflurane improves gaseous exchange and exerts a protective effect against LPS-triggered lung injury in mice model, most probably due to its anti-inflammatory and antioxidant properties

Keywords: Lung injury, Sevoflurane, Respiratory distress, Superoxide dismutase, Liposaccharide