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ABSTRACT: We investigated whether lipopolysaccharide (LPS) induced inflammation in alveolar epithelial type II (ATII) cells is through cluster of differentiation 14 (CD14) and Toll-like receptor 4 (TLR4) and the effect of different dosages of propofol on the inflammation in primary cultured rat ATII cells.
Cultured ATII cells were randomly assigned to one of the following five groups: Group C: untreated group (control) cultured in the absence of propofol and LPS; Group LPS: treated with 1 microg/ml LPS; Group P1: treated with 1 microg/ml LPS and 25 microM propofol; Group P2: treated with 1 microg/ml LPS and 50 microM propofol; Group P3: treated with 1 microg/ml LPS and 100 microM propofol. ATII cells in all groups were cultured at 37 degrees C for 3 h. CD14 and TLR4 mRNA was detected using real-time polymerase chain reaction. Western blot was used to detect CD14 and TLR4 protein expression. CD14 and TLR4 expression on the ATII cells was imaged using immunofluorescence. Tumor necrosis factor-alpha (TNF-alpha) production was determined using an ELISA kit.
LPS stimulation resulted in an increased CD14 and TLR4 expression and increased TNF-alpha production in ATII cells. Propofol, at concentrations > or = 50 microM, significantly (P<0.05) and dose-dependently decreased CD14 and TLR4 mRNA expression and protein expression in ATII cells. This was accompanied by a decrease in TNF-alpha production (P<0.05).
These results suggest that propofol, at clinically relevant concentrations, can reduce inflammatory responses in LPS-induced ATII cells injury through downregulation of CD14 and TLR4 expression.
Acta Anaesthesiologica Scandinavica 09/2009; 54(3):362-9. · 2.36 Impact Factor