Investigation Of The Effects Of Hyperoxia On Brain Tissue In Offspring Mice

Objective: In recent years,with the rapid development of medicine in China,the survival rate of premature and low weight infants is increasing.Oxygen therapy is essential for premature infants treating.When preterm infants receive oxygen therapy,high concentration of oxygen will also cause multiple organ damage to premature infants,which will have a serious impact on children and family life.High oxygen exposure can cause retinopathy,lung disease and brain damage in preterm infants.However,the specific mechanism of neonatal brain injury is not clear when exposed to high concentration oxygen.Autophagy and apoptosis are two processes of programmed cell death different from each other,mutual connection,the experimental research of the two processes are involved in high concentration oxygen exposure mice brain tissue damage caused by the process.The expression of some endogenous harmful substances produced in the body will activate the inflammasome,In this experiment,we investigate weather high concentration oxygen exposure can cause inflammation of brain tissue in mice.Method: In this experiment,C57BL/6 mice as the research object,the newborn mice at fifth days,with their mothers,were exposure to oxygen concentration of 80% in7 days,transferred to the laboratory environment and were fed for 5 days.Part ofoffspring on brain tissue dehydration embedding,slicing;DHE staining to observe the expression of ROS in fetal brain tissues change;MDA assay,detection of exposure to high oxygen content of MDA in the brain tissue of mouse offspring;using Western blot to examine the expression of apoptosis related factors,the inflammatory factors the autophagy factors and the oxidative stress factors;immunohistochemistry is examining the expression of inflammatory corpuscles in brain tissue detect.Results: After high oxygen exposure,the offspring of mice brain tissue ROS levels compared with the control group increased significantly;the results of detection of MDA content,after the high oxygen exposure,the content of MDA in brain tissue of mice was significantly higher than the control group;to determine the mechanisms involved,found high expression of Nrf2 protein in the brain of oxygen exposure increase in mice,decreasing Trx-1 protein expression,suggesting that high oxygen exposure activates oxidative stress in fetal brain tissue,causing brain injury;the expression of detecting autophagy and autophagy related factor LC3-II protein substrate protein p62,found that after exposed to hyperoxia,decreased LC3-II expression in fetal brain tissues,the expression of p62 protein obviously,suggested that hyperoxia exposure inhibited autophagy in brain tissue of mice cells;to further examine the expression of Bax and Bcl-2 in fetal brain tissues,found in hyperoxia group the ratio of Bcl-2/Bax in rat brain tissue was significantly decreased,indicating the high oxygen exposure activates apoptosis rat brain tissue;in order to further determine the brain damage in offspring mice exposed to hyperoxia,detect the expression of NLRP3 inflammasome and its downstream IL-1 beta,IL-18 experiment,found that high oxygen exposure can activate the expression of inflammatory corpuscle and its downstream factors however,cause inflammation of brain tissue.Conclusion: Hyperoxia exposure can cause brain damage in mice offspring;the inhibition of autophagy plays a key role;high oxygen can inhibit autophagy and apoptosis of elicitors to generation of mouse brain death;high oxygen exposure on the expression of inflammatory cytokines in mouse brain.