Effects of dexamethasone on cell signal transaction system ERK and PI3-K of rat with acute lung injury / 解放军医学杂志

ABSTRACT

Objective The effects of dexamethasone on cell signal transaction system ERK and PI3-K were studied in acute lung injury (ALI) rat in order to provide a theoretical basis for clinical treatment. Methods 36 healthy male SD rats were randomly divided into 3 groups, 12 rats for each group injured group, dexamethasone treated group and control group. 0.25ml/kg oleic acid was injected via caudal venous into each animal in the former two groups to form ALI models. Then, for dexamethasone treated group, each animal received 1.0mg/kg of dexamethasone 15 min after oleic acid injection; the same amount of saline was given to the animals in injured group, and the animals in control group were injected the same amount of saline at the last two times. All animals were killed by common carotid artery bleeding 2 hours after the last injection. The indexes of PaO2, wet/dry weight of left lung, pulmonary permeability and lung pathology were investigated. The expression of PI3-K, ERK and P-ERK were determined by Western blot and immunohistochemical method. Results PaO2 declined in the animals of injured group, while left lung wet/dry ratio and pulmonary permeability increased obviously, and pulmonary edema and transparent film were observed in injured lung pathology. Compared to injured group, those indexes were improved in dexamethasone treated group. PI3-K, ERK and P-ERK were highly expressed in bronchus epithelial cells, alveolar epithelial cells, pulmonary vessel endothelial cells and macrophage cells of the animals in injured group, the expression of PI3-K, ERK and P-ERK were reduced in dexamethasone group, but the expression in the both groups were still higher than that in control group. Conclusions The higher expression of PI3-K and ERK were involved in the regulation of earlier period of ALI, and dexamethasone may improve ALI by repressing the high expression of PI3-K and ERK.