Abstract:

BACKGROUND: Currently delayed encephalopathy is closely related with the cell apoptosis in nerve tissue after carbon monoxide (CO) poisoning. The protective effect of heme oxygenase-1, especially in the brain injury remains controversial.
OBJECTIVE: To observe heme oxygenase-1 mRNA and protein expression at different time points after CO poisoning in the mouse brain.
METHODS: Male Kunming mice, weighing 18-22 g, were randomly divided into CO poisoning group and air control group. The model of delayed encephalopathy after acute CO poisoning was established with intraperitoneal injection of CO. Air control group was intraperitoneally injected with air. In situ hybridization and western blot analysis were applied to observe the heme oxygenase-1 mRNA and protein expression in the hippocampus of mice in the two groups at different time points.
RESULTS AND CONCLUSION: There were few positive cells for heme oxygenase-1 mRNA expression in the air control group, with light staining; but a large number of positive cells for heme oxygenase-1 mRNA expression in CO poisoning group, with deep staining. The heme oxygenase-1 mRNA expression was increased at 1 days (P < 0.01), reached a peak at 3 days (P < 0.01), decreased at 5 days (P < 0.01), and still higher than air control group at 21 days (P < 0.01). Changes of heme oxygenase-1 protein expression were consistent with heme oxygenase-1 mRNA expression. The upregulated expression of heme oxygenase-1 mRNA and protein plays a crucial role in the pathogenesis of delayed encephalopathy after CO poisoning.

Key words: carbon monoxide poisoning, brain diseases, heme oxygenase-1, mice