Abstract:

Objective To investigate the effects of dexamethasone on the reactive oxygen species and MT⁃CO1 in lung tissues of asthma mice. Methods The asthma model was induced by egg albumin with BALB/C mice. A total of 21 BALB/C mice were randomly assigned into control group，asthma group and dexamethasone group. Biochemical kits were used to detect malondialdehyde in all the animals，and Western blot and qPCR to detect protein and mRNA expressions of MTCO1 in their lung tissues. The 16HBE cells were further divided control group，IL ⁃5 group and dexamethasone group. mitochondrial reactive oxygen species，across which mitochondrial membrane potential was detected by fluorescence and the protein and mRNA expressions of MT ⁃CO1 by Western blot and qPCR. Results The MDA in the lung tissues of the asthma group and thedexamethasone group was sig⁃ nificantly higher than that in the control group（P < 0.05），and the MDA in thedexamethasone group was higher than that in the asthma group. The mRNA expression of MT⁃CO1 in the asthma group and thedexamethasone group was significantly higher than that in the control group（P < 0.05）. The mRNA expression of MT⁃CO1 in the dexa⁃ methasone group was significantly higher than that in the asthma group（P < 0.05）and the westernblot showedthe same scenarioas qPCR. The MT⁃CO1 mRNA expression in the 16HBE，dexamethasone group and IL⁃5 group was significant decreased than that in the control group，and the express in the dexamethasone groupwas even lower than that in the IL⁃5 group but without significant. The mitochondrial reactive oxygen species in the 16HBE：dexa⁃methasone group and IL⁃5 group were significant increased than those in the control group，and the species in the dexamethasone groupwere increased to a higher extent than in the IL⁃5 group. The mitochondrial membrane poten⁃ tial in 16HBE：dexamethasone group and IL ⁃ 5 group were more significantly decreased than that in the control group，andthe potential in the dexamethasone groupwas increased to a higher extent than that in the IL ⁃ 5 group. Conclusion Dexamethasone can reduce the expression of MT⁃CO1 and further increase the level of reactive oxy⁃ gen species in lung tissue of asthmamice. Our result suggest that glucocorticoid can boost oxidative stress through mitochondrion dysfunction，which would be risk factor for irregular relapse of asthma. Antioxidation might alleviate detrimental effects of asthma through mitochondrion dysfunction caused by glucocorticoids. 

Key words:

asthma, dexamethasone, reactiveoxygenspecies, mitochondrial respiratory chain gene, oxidative stress, immune inflammation, mice