Protective function of dexmedetomidine on the oxidative stress injury induced by lung ischemia-reperfusion in rats
10.13699/j.cnki.1001-6821.2017.13.015
- VernacularTitle:右美托咪定对大鼠肺缺血再灌注引起的氧化应激损伤的保护作用
- Author:
Feng-Ying SUN
1
;
Dong-Mei ZHANG
;
Guang YAO
;
Xiang-Mei BU
Author Information
1. 滨州医学院附属医院麻醉科
- Keywords:
dexmedetomidine pretreatment;
lung oxidative stress injury;
nuclear factor E2-related factor 2
- From:
The Chinese Journal of Clinical Pharmacology
2017;33(13):1221-1224
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of dexmedetomidine pretreatment on rat lung oxidative stress injury induced by ischemia-reperfusion (I/R).Methods The model of lung I/R injury was established by clamping the hilum of left lung for 45 min followed by reperfusion.Twenty-four SD rats were randomly divided into sham group,model group,and experiment group.Each group had eight rats.Rats in the sham group were underwent left thoracotomies with no I/R.Rats were received normal saline or dexmedetomidine at a rate of 3.0 μg · kg-1 · h-1 for 60 min in the model group or experiment group before ischemia,respectively.After reperfusion of 120 min,blood sample from left pulmonary vein was collected for blood gas analysis.HE staining was used to evaluate lung injury score (LIS).Xanthine oxidase method and thiobarbituric acid method were used to detected superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in the left lung tissues,respectively.Western Blot was used to detected nuclear factor E2-related factor 2 (Nrf2) protein expression of left lung tissue.Results Compared with the sham group of LIS 3.5 ± 0.6,MDA content (1.6 ± 0.3) nmol · mg-1,SOD activity (65.1 ± 4.8) U · mg-1,the LIS 8.5 ± 1.3 and MDA content (5.8 ± 2.2) nmol · mg-1 in model group increased significantly;while the SOD activity (30.3 ± 4.1) U · mg-1 in the model group decreased significantly (P ＜ 0.05).Compared with the model group,LIS (5.0 ± 1.2) and MDA content (2.7 ± 0.3) nmol · mg-1 in experiment group reduced significantly(P ＜ 0.05),while SOD activity (61.4 ± 1.9) U · mg-1 in experiment group increased significantly also (P ＜ 0.05).Compared with the sham group on nuclear Nrf2 protein expression of 0.25 ± 0.04,nuclear Nrf2 protein expression in the model group decreased with 0.12 ± 0.02,which had significant difference (P ＜ 0.05).Compared with the model group,the nuclear Nrf2 protein expression in the experiment group increased of 0.53 ± 0.05,which showed significant difference (P ＜ 0.05).Conclusion Dexmedetomidine pretreatment decreased the MDA content and increased the SOD activity via activating Nrf2 pathway,and ameliorated lung oxidative stress induced by I/R and improved lung function.
