| BackgroundThe birth rate of premature infants in the world has increased year by year.The birth rate of premature infants in China has risen from 5%in 1980 to 10%in 2022.At present,more than 1 million premature infants are born every year.Oxygen therapy can not be avoided in the early treatment of premature infants,and more attention has been paid to brain damage caused by oxygen therapy.Clinical studies and animal experiments over the past decade have shown that normobaric hyperoxia can lead to white matter and gray matter damage in premature infants through oxidative stress and inflammation.In the mature period of the brain,hyperoxia can affect its development,including the destruction of neural plasticity and myelination in the early stage,and may affect motor and cognitive function in the long term.Therefore,how to prevent brain injury in premature infants with normobaric hyperoxia is particularly important.ObjectiveWe investgated whether astragalus polysaccharides(APS)can reduce brain injury in newborn rats with normobaric hyperoxia.Methods1.Establish animal model:40 newborn 3-day-old(P3)SD rats were randomly divided into 4 groups(n=10):air+saline group(group A),air+astragalus polysaccharide group(40mg/kg·d:group B),hyperoxia+saline group(group C),hyperoxia+astragalus polysaccharide group(40mg/kg·d:D group).The rats of group C and group D were exposed to 80%concentration of oxygen for 24 hours to establish a newborn rat model of brain damage.2.On the 3rd day after hyperoxia(P6),the brain tissue was taken for HE staining,Tunel to detect apoptosis,inflammatory factors(IL-1β,IL-6),oxidative stress(Total superoxide dismutase T-SOD),and WB to detect EGFL7 protein expression in brain tissue.Results:1.Compared with the control group(group A),the HE staining of brain tissue sections in the normobaric hyperoxia brain injury model group(group C)showed more white matter cell edema,nuclear pyknosis and disordered tissue arrangement;compared with group C,the tissue arrangement in group D was more orderly.2.After hyperoxia on the third day(P6),the apoptosis index of group C was higher than that of the control group A(P<0.05);the apoptosis index of group C was higher than that of group B(P<0.05);the apoptosis index of group D was lower than that of group C(P<0.05);the apoptosis index of group D was higher than that of group B Significant(P<0.05).3.After hyperoxia for 3 days(P6),there was no significant difference in brain inflammatory factors(IL-1β,IL-6)among the three groups.4.After hyperoxia for 3 days(P6),the concentration of T-SOD in group D was significantly higher than that in group A(P<0.05),the concentration of T-SOD in group D was significantly higher than that in group B(P<0.05),and the concentration of T-SOD in group D was significantly higher than that in group C(P<0.05).The concentration of T-SOD in group B was significantly higher than that in group C(P<0.05).5.After hyperoxia for 3 days(P6),the concentration of EGFL7 protein in group D was significantly higher than that in group C,the concentration of EGFL7 protein in group C was significantly lower than that in group A(P<0.05),and the concentration of EGFL7 protein in group C was significantly lower than that in group B(P<0.05).Conclusion1.Astragalus polysaccharides(APS)can reduce brain injury in neonatal rats exposed to normobaric hyperoxia by up-regulating EGFL7 and increasing the activity of superoxide dismutase(SOD).2.Injection of astragalus polysaccharides(40mg/kg·d)alone with neonatal rats did not increase apoptosis,oxidative stress and inflammation in brain tissue.3.In the short term(within 3 days),brain tissue of neonatal rats usually do not cause inflammatory response to hyperoxia. |
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