The effect of cyclosporine A on lipopolysaccharide-induced acute lung injury in mice.
- Author:
Jun-Feng HU
1
;
Xue-Mei XIA
;
Dian-Ming LI
;
Yong ZHANG
;
Yu-Qing CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Acute Lung Injury; chemically induced; physiopathology; prevention & control; Animals; Cyclosporine; pharmacology; L-Lactate Dehydrogenase; metabolism; Lipopolysaccharides; Male; Mice; Mice, Inbred ICR; Mitochondrial Membrane Transport Proteins; antagonists & inhibitors; Protective Agents; pharmacology; Tumor Necrosis Factor-alpha; metabolism
- From: Chinese Journal of Applied Physiology 2011;27(1):120-123
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of mitochondrial permeability transition pore inhibitor cyclosporine A (CsA) on lipopolysaccharide (LPS)-induced acute lung injury in mice.
METHODSAll male ICR mice were randomly divided into five groups (n = 24): control group, LPS group, dexamethasone group, cyclosporine A(CsA) group and CsA + atractyloside(Atr) group. Six hours after treatment with LPS, the activity of lactate dehydrogenlase (LDH) in bronchoalveolar lavage fluid (BALF) and level of tumor necrosis factor-alpha (TNF-alpha) in lung tissue were detected. The lung wet weight/dry weight ratio and the pulmonary capillary permeability index were also detected.
RESULTSIn contrast to LPS group, the mitochondrial permeability transition pore inhibitor CsA induced a decrease in LDH activity in the BALF and TNF-alpha level in lung tissue, lung wet weight/dry weight ratio and the pulmonary capillary permeability index were declined. Atractyloside, the activator of mitochondrial permeability transition pore, almost abolished the role of CsA on LPS-induced lung injury.
CONCLUSIONThese results suggested that CsA plays the protective effect on LPS-induced lung injury in mice, it is likely through inhibiting the opening of mitochondrial permeability transition pore.
