2011Zhongguo bingli shengli zazhiRequires access

Paeoniflorin attenuates LPS-induced acute lung injury in mice

Yiyang Wang

Open publisher page 1 citations

Abstract

AIM:To investigate the mechanisms by which paeoniflorin(Pae) attenuates lipopolysaccharide(LPS)-induced acute lung injury in mice.METHODS: Male BALB/c mice were randomly divided into 4 groups: control,LPS,Pae+LPS,and Pae.Mice were administered intragastrically with double distilled water or Pae(20 mg/kg) once a day for 3 days.One hour after intragastrical treatment on the third day,LPS(20 mg/kg) or normal saline was injected intraperitoneally.Twelve hours after LPS challenge,the histological changes of the lung were observed,and histology score was also assessed.The myeloperoxidase(MPO),cytosolic phospholipase A2(cPLA2) and phosphorylated cytosolic phospholipase A2(phospho-cPLA2) in lung tissues were detected by Western blotting.RESULTS: LPS challenge resulted in acute lung injury,activated cPLA2 and increased MPO content in lung.Pretreatment with paeoniflorin significantly attenuated lung injury induced by intraperitoneal injection of LPS.The levels of MPO and phospho-cPLA2 in the lung tissues of the mice in Pae+LPS group were lower than those in LPS group(P0.05).CONCLUSION: Pretreatment with paeoniflorin remarkably reduces LPS-induced acute lung injury through inhibiting phosphorylation of cPLA2 and decreasing neutrophil infiltration in the lung.These findings provide a new strategy for the prevention and treatment of LPS-induced acute lung injury.

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AIM:To investigate the mechanisms by which paeoniflorin(Pae) attenuates lipopolysaccharide(LPS)-induced acute lung injury in mice.METHODS: Male BALB/c mice were randomly divided into 4 groups: control,LPS,Pae+LPS,and Pae.Mice were administered intragastrically with double distilled water or Pae(20 mg/kg) once a day for 3 days.One hour after intragastrical treatment on the third day,LPS(20 mg/kg) or normal saline was injected intraperitoneally.Twelve hours after LPS challenge,the histological changes of the lung were observed,and histology score was also assessed.The myeloperoxidase(MPO),cytosolic phospholipase A2(cPLA2) and phosphorylated cytosolic phospholipase A2(phospho-cPLA2) in lung tissues were detected by Western blotting.RESULTS: LPS challenge resulted in acute lung injury,activated cPLA2 and increased MPO content in lung.Pretreatment with paeoniflorin significantly attenuated lung injury induced by intraperitoneal injection of LPS.The levels of MPO and phospho-cPLA2 in the lung tissues of the mice in Pae+LPS group were lower than those in LPS group(P0.05).CONCLUSION: Pretreatment with paeoniflorin remarkably reduces LPS-induced acute lung injury through inhibiting phosphorylation of cPLA2 and decreasing neutrophil infiltration in the lung.These findings provide a new strategy for the prevention and treatment of LPS-induced acute lung injury.

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Available abstract

AIM:To investigate the mechanisms by which paeoniflorin(Pae) attenuates lipopolysaccharide(LPS)-induced acute lung injury in mice.METHODS: Male BALB/c mice were randomly divided into 4 groups: control,LPS,Pae+LPS,and Pae.Mice were administered intragastrically with double distilled water or Pae(20 mg/kg) once a day for 3 days.One hour after intragastrical treatment on the third day,LPS(20 mg/kg) or normal saline was injected intraperitoneally.Twelve hours after LPS challenge,the histological changes of the lung were observed,and histology score was also assessed.The myeloperoxidase(MPO),cytosolic phospholipase A2(cPLA2) and phosphorylated cytosolic phospholipase A2(phospho-cPLA2) in lung tissues were detected by Western blotting.RESULTS: LPS challenge resulted in acute lung injury,activated cPLA2 and increased MPO content in lung.Pretreatment with paeoniflorin significantly attenuated lung injury induced by intraperitoneal injection of LPS.The levels of MPO and phospho-cPLA2 in the lung tissues of the mice in Pae+LPS group were lower than those in LPS group(P0.05).CONCLUSION: Pretreatment with paeoniflorin remarkably reduces LPS-induced acute lung injury through inhibiting phosphorylation of cPLA2 and decreasing neutrophil infiltration in the lung.These findings provide a new strategy for the prevention and treatment of LPS-induced acute lung injury.

Key concepts: Paeoniflorin, Myeloperoxidase, Lipopolysaccharide, Lung, Medicine, Pharmacology, Phospholipase A2, Saline

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