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Effects of silymarin on LPS-induced acute lung injury in rats / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12)1986.
Artigo em Chinês | WPRIM | ID: wpr-528910
ABSTRACT

AIM:

To investigate the effects of silymarin on lipopolysaccharide(LPS)-induced acute lung injury in rats and its possible molecular mechanisms.

METHODS:

Fifty-eight male SD rats,weighting 230-250 g,were divided into four groups randomly normal control(n=12);acute lung injury group(n=15),receiving intravenous LPS(O55∶B5,5 mg/kg);silymarin alone group(50 mg/kg,n=15);intervention group(n=16,receiving silymarin 50 mg/kg and LPS 5 mg/kg).The specimens were collected 6 hours later.The following changes,including blood gas analysis,the lung wet/dry weight ratio,the pulmonary vascular permeability,histological manifestations,lung tissue myeloperoxidase activity,the levels of TNF-?,IL-1?,MCP-1 and SOD,GSH-Px as well as malonaldehyde and conjugated diene in plasma and lung tissue,were observed.

RESULTS:

Compared with control group,the lungs of the rats in LPS treatment group showed significant hyperemia and spotted hemorrhage.The inflammatory granulocyte infiltrating,diffused alveolar septum thickening and spotted hemorrhage were observed in pathological examinations.The lung wet/dry weight ratio and Evans blue content(per gram) increased significantly after LPS treatment.The myeloperoxidase activity in plasma and lung tissue,the levels of TNF-?,IL-1?,MCP-1 and SOD,GSH-Px as well as malonaldehyde and conjugated diene were increased significantly in LPS treatment group.However,in intervention groups,all the above-mentioned measurements were reversed significantly by silymarin treatment compared with LPS treatment group.

CONCLUSION:

Silymarin may decrease inflammatory reaction and oxidative stress,and further decrease lung damage induced by LPS in rats,all indicating protection of silymarin against acute lung injury.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 1986 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 1986 Tipo de documento: Artigo