Research Papers:

Dexmedetomidine alleviates lipopolysaccharide-induced lung injury in Wistar rats

Xuetao Yan _, Xiaoli Cheng, Liwen Zhou, Xianghu He, Wenzhong Zheng and Hu Chen

PDF  |  HTML  |  How to cite

Oncotarget. 2017; 8:44410-44417. https://doi.org/10.18632/oncotarget.17899

Metrics: PDF 1435 views  |   HTML 2385 views  |   ?  


Xuetao Yan1, Xiaoli Cheng2, Liwen Zhou3, Xianghu He4, Wenzhong Zheng1 and Hu Chen1

1Department of Anesthesiology, Shenzhen Bao’an Maternity and Child Health Hospital, Shenzhen, 518100, China

2Department of Pharmacy, Shenzhen Bao’an Maternity and Child Health Hospital, Shenzhen, 518100, China

3Department of Anesthesiology, Xiangyang Central Hospital, Xiangyang, 441021, China

4Department of Anesthesiology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China

Correspondence to:

Xuetao Yan, email: [email protected]

Keywords: dexmedetomidine, lung injury, inflammation, oxidative stress, Nrf2

Received: April 07, 2017     Accepted: April 27, 2017     Published: May 16, 2017


This study aimed to investigate the protective effects of dexmedetomidine on lipopolysaccharide (LPS)-induced lung injury in Wistar rats. 24 female Wistar rats were randomly assigned into 3 groups (n = 8): a control group, a LPS-challenged group, and a LPS plus dexmedetomidine group. Inflammation, oxidative stress, Nrf2/Keap1, and Akt signal were determined. The results showed that LPS caused inflammation and oxidative stress via increasing pro-inflammatory cytokines and oxidative products. Dexmedetomidine treatment alleviated inflammation and oxidative stress in LPS-challenged rats. Nrf2/Keap1 was inhibited and Akt signal was activated in the lung after exposure to LPS, while dexmedetomidine activated Nrf2/Keap1, which further mediated expressions of antioxidant genes. In conclusion, dexmedetomidine alleviated inflammatory response and oxidative stress in LPS-induced lung injury in rats via influencing Nrf2/Keap1 signal.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 17899