Objective: To investigate the effect of dexamethasone on the expression of fractalkine (FKN) in lipopolysaccharide (LPS)-induced acute lung injury (ALI).
Methods: The rat model of ALI was established by injection of LPS at the dose of 4 mg/kg. 42 Wistar rats were randomly divided into the normal group (n=6), LPS group (n=18), and dexamethasone (DEX) group (n = 18), and then the rats in both LPS and DEX groups were divided into three subgroups (1 h, 2 h and 4 h after injection of LPS), respectively. The pathological condition and the wet/dry ratio (W/D) of the lung were observed, and serum TNF-alpha level, and FKN mRNA of the lung were detected with ELISA and RT-PCR.
Results: The W/D, serum TNF-alpha level, and FKN mRNA of the lung were significantly increased in LPS group, compared with those in normal group (all P < 0.05), but the W/D, serum TNF-alpha level, and FKN mRNA of the lung in the DEX group were much more decreased than those in the LPS group (all P < 0.05). In addition, the expression of FKN mRNA in the lung tissue positively correlated with the concentration of TNF-alpha (r = 0.674, P <0.05).
Conclusion: The findings suggested that pre-treatment with dexamethasone could inhibit the TNF-alpha level and prevent the increase of the expression of FKN mRNA, which may be one of the mechanisms by which DEX serves as a protection against LPS-induced lung injury.