右美托咪定减轻脂多糖诱导的Wistar大鼠肺损伤。
Dexmedetomidine alleviates lipopolysaccharide-induced lung injury in Wistar rats.
作者信息
Yan Xuetao, Cheng Xiaoli, Zhou Liwen, He Xianghu, Zheng Wenzhong, Chen Hu
机构信息
Department of Anesthesiology, Shenzhen Bao'an Maternity and Child Health Hospital, Shenzhen, 518100, China.
Department of Pharmacy, Shenzhen Bao'an Maternity and Child Health Hospital, Shenzhen, 518100, China.
出版信息
Oncotarget. 2017 Jul 4;8(27):44410-44417. doi: 10.18632/oncotarget.17899.
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.
本研究旨在探讨右美托咪定对脂多糖（LPS）诱导的Wistar大鼠肺损伤的保护作用。将24只雌性Wistar大鼠随机分为3组（n = 8）：对照组、LPS攻击组和LPS加右美托咪定组。检测炎症、氧化应激、Nrf2/Keap1和Akt信号。结果表明，LPS通过增加促炎细胞因子和氧化产物导致炎症和氧化应激。右美托咪定治疗减轻了LPS攻击大鼠的炎症和氧化应激。暴露于LPS后，肺组织中Nrf2/Keap1被抑制，Akt信号被激活，而右美托咪定激活Nrf2/Keap1，进而介导抗氧化基因的表达。总之，右美托咪定通过影响Nrf2/Keap1信号减轻了LPS诱导的大鼠肺损伤中的炎症反应和氧化应激。
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