Year: 2017
Type: article
Abstract: // Xuetao Yan 1 , Xiaoli Cheng 2 , Liwen Zhou 3 , Xianghu He 4 , Wenzhong Zheng 1 and Hu Chen 1 1 Department of Anesthesiology, Shenzhen Bao’an Maternity and Child Health Hospital, Shenzhen, 518100, China 2 Department of Pharmacy, Shenzhen Bao’an Maternity and Child Health Hospital, Shenzhen, 518100, China 3 Department of Anesthesiology, Xiangyang Central Hospital, Xiangyang, 441021, China 4 Department 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 ABSTRACT 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.
Source: Oncotarget
Language: English
Subfield: Anesthesiology and Pain Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: diamond
OpenAlex ID: W2614716166