Protective Effect Of Vitexin On Acute Lung Injury In Mice

Objective:To investigate the effect of vitexin on lipopolysaccharide-induced acute lung injury in mice.Methods:Lipopolysaccharide (LPS,7mg/kg) was injected through the abdominal cavity to induce acute lung injury. Seventy-two male C57BL /6 mice were randomly divided into 6 groups:normal group, vitexin control group, model group, vitexin low dose group (0.3 mg/kg), vitexin middle dose group (1 mg/kg), vitexin high dose group (3 mg/kg). Conditions were observed. After 6 hours in a broken neck death in mice, the ratio of wet to dry lung tissue weight(W/D) and the contents of tumor necrosis factor-alpha (TNF-α), superoxide dismutase (SOD), malondialdehyde (MDA) in lung tissues were determined. The levels of total protein in alveolar lavage fluid were detected. The histopathological changes of lung tissues were observed under light microscope.The expression of NF-κBp65mRNA were measured.Results:Compared with normal group, depression, move slowly, not eating and secreation increased were observed in model group. The typical pathological changes of lung injury were presented in pathological section in model group.The contents of TNF-α,MDA in lung tissues, the levels of total protein in alveolar lavage fluid, the lung wet/dry weight ratio, the expression of NF-KBp65mRNA were increased significantly (P< 0.05) Thecontents of SOD were decreased significantly (P<0.05).Compared with model group, the conditions of mice,the pathological injury were inproved, the contents of TNF-a,MDA in lung tissues, the levels of total protein in alveolar lavage fluid were decreased significantly in the low,middle,high groups (P<0.05). The contents of SOD were increased, the lung wet/dry weight ratio were decreased in the middle, high groups (P <0.05).The expression of NF-kBp65mRNA were down-regulated in the low,middle,high groups (P<0.05)Conclusion:Vitexin has protective effect on acute lung injury in mice through anti-inflammatory, antioxidant effect which probably associated with the inhibition of the expression of NF-KBp65mRNA.