2010Journal of Ningxia Medical UniversityRequires access

Changes of Lung Injury Indices and Serum Inflammatory Factors in Mice with Endotoxemia Induced by Lipopolysaccharide

Lin Huang

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Abstract

Objective To establish the endotoxemia model induced by lipopolysaccharide(LPS) in mice,and to observe the changes of lung injury indices and serum inflammatory factors.Methods The BALB/c mice were divided into two groups randomly,normal control group and LPS-induced model group.Each group was further divided into four subgroups by time control point.General symptoms were recorded.Histopathological changes in lung was observed and lung wet/dry weight were measured.Serum TNF-α and NO were measured by using radio immunoassay and nitrate reductase method.Results(1) Symptoms appeared at 30min after LPS injection on mice in LPS-induced model group and continued within 24h;pathological change was distinct in every time-control-point.The lung tissue pathological changes aggravated at 6h and continued within 24h.Lung wet/dry weight significantly increased in model group compared to that in controls.The levels of serum TNF-α and NO increased at 2h after LPS administration,peaked at 6h and 12h,then declined.The levels of serum TNF-α and NO sustained higher in model group than those in control group at 24h(P0.01).Conclusion 7mg·kg-1 LPS with intravenous injection can establish an ideal animal model of acute lung injury;uncontrolled expression of inflammatory mediators is one of an important mechanism in LPS-induced acute lung injury.

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Objective To establish the endotoxemia model induced by lipopolysaccharide(LPS) in mice,and to observe the changes of lung injury indices and serum inflammatory factors.Methods The BALB/c mice were divided into two groups randomly,normal control group and LPS-induced model group.Each group was further divided into four subgroups by time control point.General symptoms were recorded.Histopathological changes in lung was observed and lung wet/dry weight were measured.Serum TNF-α and NO were measured by using radio immunoassay and nitrate reductase method.Results(1) Symptoms appeared at 30min after LPS injection on mice in LPS-induced model group and continued within 24h;pathological change was distinct in every time-control-point.The lung tissue pathological changes aggravated at 6h and continued within 24h.Lung wet/dry weight significantly increased in model group compared to that in controls.The levels of serum TNF-α and NO increased at 2h after LPS administration,peaked at 6h and 12h,then declined.The levels of serum TNF-α and NO sustained higher in model group than those in control group at 24h(P0.01).Conclusion 7mg·kg-1 LPS with intravenous injection can establish an ideal animal model of acute lung injury;uncontrolled expression of inflammatory mediators is one of an important mechanism in LPS-induced acute lung injury.

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Available abstract

Objective To establish the endotoxemia model induced by lipopolysaccharide(LPS) in mice,and to observe the changes of lung injury indices and serum inflammatory factors.Methods The BALB/c mice were divided into two groups randomly,normal control group and LPS-induced model group.Each group was further divided into four subgroups by time control point.General symptoms were recorded.Histopathological changes in lung was observed and lung wet/dry weight were measured.Serum TNF-α and NO were measured by using radio immunoassay and nitrate reductase method.Results(1) Symptoms appeared at 30min after LPS injection on mice in LPS-induced model group and continued within 24h;pathological change was distinct in every time-control-point.The lung tissue pathological changes aggravated at 6h and continued within 24h.Lung wet/dry weight significantly increased in model group compared to that in controls.The levels of serum TNF-α and NO increased at 2h after LPS administration,peaked at 6h and 12h,then declined.The levels of serum TNF-α and NO sustained higher in model group than those in control group at 24h(P0.01).Conclusion 7mg·kg-1 LPS with intravenous injection can establish an ideal animal model of acute lung injury;uncontrolled expression of inflammatory mediators is one of an important mechanism in LPS-induced acute lung injury.

Key concepts: Lipopolysaccharide, Lung, Medicine, Pathological, Inflammation, Tumor necrosis factor alpha, Internal medicine, Animal model

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