2013China Modern MedicineRequires access

The effect and mechanism study of oxygen free radical scavenger on nuclear factor-κB in rat acute lung injury

Wang Tin

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Abstract

Objective To explore the effect and mechanism of oxygen free radical scavenger edaravone on nuclear factor-κB of in rat acute lung injury induced by lipopolysaccharide.Methods 30 male SD rats were evenly and randomly divided into three groups:control group(group A),model group(group B),and edaravone group(group C).In group B and group C,5 mg/kg lipopolysaccharide was injected in peritoneal cavity respectively for modeling.In group A,5 mg/kg of 0.9% sodium chloride injection was injected in abdominal cavity as control group.After modeling,in group C,intraperitoneal injection of 10 ml/kg edaravone was performed for intervention.The intraperitoneal injection of 10 ml/kg in 0.9% sodium chloride injection was carried out in both group A and group B for comparisons.These rats were killed after 6 hours.The blood oxygen pressure(PO2) was measured by blood gas analysis after blood being extracted from abdominal aorta,the content of nuclear factor-κB in lung tissue was determined by immunohistochemistry,and the content of TNF-α was tested by ELISA.Results The PO2 of rats in both group B and C were lower than that in group A with statistical difference(P0.05).The descending range of PO2 in group C was less than that in group B.In comparison with group B,the PO2 in group C was higher with statistical difference(P0.05).The contents of nuclear factor-κB and TNF-α of rats in group B and C were higher than those in group A with statistical differences(P0.05).The ascending range of nuclear factor-κB and TNF-α in group C was less than those in group B.Compared with group B,the contents of nuclear factor-κB and TNF-α in group C were lower,which displayed statistical differences(P0.05).Conclusion Edaravone has the protective effect on lung tissue of rat in acute lung injury caused by lipopolysaccharide,and is related with inhibition of NF-κB expression in lung tissue and inhibition of pulmonary inflammatory response accordingly.

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Objective To explore the effect and mechanism of oxygen free radical scavenger edaravone on nuclear factor-κB of in rat acute lung injury induced by lipopolysaccharide.Methods 30 male SD rats were evenly and randomly divided into three groups:control group(group A),model group(group B),and edaravone group(group C).In group B and group C,5 mg/kg lipopolysaccharide was injected in peritoneal cavity respectively for modeling.In group A,5 mg/kg of 0.9% sodium chloride injection was injected in abdominal cavity as control group.After modeling,in group C,intraperitoneal injection of 10 ml/kg edaravone was performed for intervention.The intraperitoneal injection of 10 ml/kg in 0.9% sodium chloride injection was carried out in both group A and group B for comparisons.These rats were killed after 6 hours.The blood oxygen pressure(PO2) was measured by blood gas analysis after blood being extracted from abdominal aorta,the content of nuclear factor-κB in lung tissue was determined by immunohistochemistry,and the content of TNF-α was tested by ELISA.Results The PO2 of rats in both group B and C were lower than that in group A with statistical difference(P0.05).The descending range of PO2 in group C was less than that in group B.In comparison with group B,the PO2 in group C was higher with statistical difference(P0.05).The contents of nuclear factor-κB and TNF-α of rats in group B and C were higher than those in group A with statistical differences(P0.05).The ascending range of nuclear factor-κB and TNF-α in group C was less than those in group B.Compared with group B,the contents of nuclear factor-κB and TNF-α in group C were lower,which displayed statistical differences(P0.05).Conclusion Edaravone has the protective effect on lung tissue of rat in acute lung injury caused by lipopolysaccharide,and is related with inhibition of NF-κB expression in lung tissue and inhibition of pulmonary inflammatory response accordingly.

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Available abstract

Objective To explore the effect and mechanism of oxygen free radical scavenger edaravone on nuclear factor-κB of in rat acute lung injury induced by lipopolysaccharide.Methods 30 male SD rats were evenly and randomly divided into three groups:control group(group A),model group(group B),and edaravone group(group C).In group B and group C,5 mg/kg lipopolysaccharide was injected in peritoneal cavity respectively for modeling.In group A,5 mg/kg of 0.9% sodium chloride injection was injected in abdominal cavity as control group.After modeling,in group C,intraperitoneal injection of 10 ml/kg edaravone was performed for intervention.The intraperitoneal injection of 10 ml/kg in 0.9% sodium chloride injection was carried out in both group A and group B for comparisons.These rats were killed after 6 hours.The blood oxygen pressure(PO2) was measured by blood gas analysis after blood being extracted from abdominal aorta,the content of nuclear factor-κB in lung tissue was determined by immunohistochemistry,and the content of TNF-α was tested by ELISA.Results The PO2 of rats in both group B and C were lower than that in group A with statistical difference(P0.05).The descending range of PO2 in group C was less than that in group B.In comparison with group B,the PO2 in group C was higher with statistical difference(P0.05).The contents of nuclear factor-κB and TNF-α of rats in group B and C were higher than those in group A with statistical differences(P0.05).The ascending range of nuclear factor-κB and TNF-α in group C was less than those in group B.Compared with group B,the contents of nuclear factor-κB and TNF-α in group C were lower,which displayed statistical differences(P0.05).Conclusion Edaravone has the protective effect on lung tissue of rat in acute lung injury caused by lipopolysaccharide,and is related with inhibition of NF-κB expression in lung tissue and inhibition of pulmonary inflammatory response accordingly.

Key concepts: Medicine, Edaravone, Group B, Free radical scavenger, Lipopolysaccharide, Intraperitoneal injection, Group A, Lung

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