Chinese Journal Of Clinical Anatomy ›› 2014, Vol. 32 ›› Issue (6): 711-715.doi: 10.13418/j.issn.1001-165x.2014

Previous Articles     Next Articles

Changes of heme oxygenase-1 and apoptosis as well as the relationship between them following carbon monoxide poisoning delayed encephalopathy in mice

ZHAO Lin -Yan1, LI-Fang2, WANG Su-Ping2, YU-Jian1   

  1. 1.Intensive Care Unit, The Second Hospital of Dalian Medical University, Dalian 116027, Liaoning Province, China;  2. Department of Neurology, Dalian Municipal Central Hospital, Dalian 116033, Liaoning Province, China
  • Received:2014-02-16 Online:2014-11-25 Published:2014-12-04

Abstract:

Objective To study the expression of the heme oxygenase-1 in the brain of mice at different time points after carbon monoxide poisoning. To detect neuron apoptosis and related gene expression in the brain of mice at different time points after carbon monoxide poisoning. To investigate the relationship between changes in heme oxygenase-1 and apoptosis of brain cells.  Methods Carbon monoxide poisoning delayed encephalopathy model by using intraperitoneal injection of carbon monoxide. Application The expression of HO-1 protein levels was observed By Western blotting analysis. Flow cytometry was used to detect apoptotic cells. Application immunohistochemistry SABC observed Bcl-2 and Bax expression at the protein level. Results Expression of HO-1 protein is less in the air Control group by Western blotting;expression increased at 1d (1.14±0.43) (P<0.01), reaching a peak at 3d (2.91±1.07) (P<0.01) in CO poisoning group;Expression of HO-1 protein in poisoning group was still higher than in that in the control group at 21d (P<0.01). Apoptosis: the percentage of apoptotic cells increased in CO poisoning 12h group (21.95±24) (P<0.01), reaching the peak at 5d (34.27±4.19) (P< 0.01). The percentage of apoptotic cells was still high at 21d (9.25±1.16). Protein related: Bax expression increased after the poisoning, reaching the peak at 3d (34.5±0.58)( P<0.01). Bcl-2 expression reduced to a minimum at 3d (12.5±3.69) (P<0.01). The ratio of Bax/Bcl-2 reached maximum at 3d. Conclusion Expression of heme oxygenase-1 protein and Apoptotic cells were significantly increased in the hippocampus after delayed encephalopathy in mouse of carbon monoxide poisoning. The changes of apoptotic cells were consistent with heme oxygenase-1 protein expression. The upregulated expression of heme oxygenase-1 protein plays a crucial role in the pathogenesis of delayed encephalopathy after CO poisoning.

Key words: Carbon monoxide poisoning, Hemeoxygenase-1, Neural apoptosis, Apoptosis gene, Mice

CLC Number: