The effects of vitamin E and dexamethasone on inflammation of acute lung injury and expression of myosin light chain kinase

2009 
OBJECTIVE: To observe the effect of vitamin E (VitE) combined with dexamethasone (DXM) on inflammation of acute lung injury and expression of myosin light chain kinase. METHODS: Forty female Balb/c mice were randomly divided into 4 groups, a saline control group (1.5 ml/kg), a LPS group (1 mg/kg), a VitE and DXM group (VitE 50 mg/kg, DXM 1 mg/kg), and a VitE group (50 mg/kg). Lung tissue histopathological changes were observed. Immunohistochemistry assays (SABC) were used to determine the myosin light chain kinase (MLCK) immunoreactive cells in the lung tissues, and the MLCK mRNA and the MLCK protein was assayed by RT-PCR and by Western blot, respectively. Means were compared with analysis of variance and Student-Newman-Keuls were used to compare 2 means. RESULTS: Histological examination showed that extensive lung inflammation were seen in the LPS group, which manifested by accumulation of significant numbers of neutrophils, accompanied by marked pulmonary edema and hemorrhage. The inflammation and hemorrhage in the 2 treatment groups were significantly improved. Immunoreactive cells of MLCK numbers in BALF in the control group, the LPS group, the VitE and DXM group, and the VitE group was (1.1 +/- 0.4), (5.6 +/- 2.1), (4.0 +/- 1.0), (4.2 +/- 1.3) x 10(9)/L respectively. Compared with other groups, the difference of LPS group was significant (F = 14. 53, all P 0.05). Compared with LPS group, the difference of A values of MLCK protein of lung tissue in two treatment groups was statistical significance (F = 12.06, all P < 0.01). CONCLUSIONS: Vitamin E combined with low dose of DXM could effectively inhibit inflammation and expression of MLCK protein in acute lung injury induced by LPS lung. It is suggested that, inhibition of MLCK activation leads to stabilize vascular barrier function and attenuation of pulmonary edema and inflammation, which also suggests a possible role of MLCK in the pathogenesis of acute lung injury.
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