Neuroprotective effect and mechanism of edaravone on brain injury following carbon monoxide poisoning
10.3760/cma.j.issn.1671-8925.2015.08.011
- VernacularTitle:依达拉奉对一氧化碳中毒后脑损伤的神经保护作用及机制研究
- Author:
Qin LI
1
;
Yongmei CHENG
;
Mingjun BI
;
Hai KANG
;
Yong ZOU
Author Information
1. 青岛大学医学院附属烟台毓璜顶医院急救中心
- Keywords:
Carbon monoxide poisoning;
Edaravone;
Apoptosis;
Oxidative stress;
Heme oxygenase-1;
Nuclear factor erythrocyte two related factor-2
- From:
Chinese Journal of Neuromedicine
2015;14(8):810-816
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the neuroprotective effect of edaravone on brain tissues after acute carbon monoxide (CO) poisoning and explore its mechanism.Methods Ninety Sprague-Dawley rats were randomly selected as normal control group,poisoning group and treatment group (n=30).Rats in the poisoning group and treatment group were established animal models of acute CO poisoning with hyperbaric chamber method and received hyperbaric oxygen therapy.The rats in the treatment group were given intraperitoneal injection ofedaravone (10 mg/kg) additionally.TUNEL and real time-PCR were used to detect the cell apoptosis and their apoptosis-related gene expressions (Bcl-2 and Bax mRNA) in brain tissues 1,2 and 7 d after CO poisoning in each group.Immunohistochemistry and Western blotting were used to observe the positive cells and protein changes of heme oxygenase-1 (HO-1) and nuclear factor erythrocyte two related factors-2 (NRF-2).Results The apoptosis cell number in the poisoning group and the treatment group was significantly increased as compared with that in the normal control group (P＜0.05);that in the treatment group was relatively fewer than that in the poisoning group with significant differences (P＜0.05).As compared with those in the normal control group,the Bcl-2 and Bax mRNA expressions in the poisoning group were obviously up-regulated with significant difference (P＜0.05);the Bcl-2 mRNA level was significantly increased,the Bax mRNA level was signficantly down-regulated,and the ratio ofBcl-2 mRNA/Bax mRNA was notablyly increased in the treatment group as compared with those in the poisoning group (P＜0.05).The positive cells and HO-1 and NRF-2 proteins in the brain tissues of the poisoning group were significantly higher than those in the normal group (P＜0.05);those in the treatment group were obviously increased as compared with those in the poisoning group (P＜0.05).Conclusion Edaravone might be partly associated with activation of NRF-2/HO-1 pathway to counteract oxidative stress damage,inhibit neuronal apoptosis,and play a neuroprotective role in brain damage after acute CO poisoning.
