| Objective To investigate the effects of lidocaine on expression of factors of inflammation induced by lipopolysaccharide in rat alveolar type II epithelial cells.Methods Alveolar type II epithelial cells were isolated from adult male SD rats, purified and incubated The cells were randomly divided into four groups:group I control; group II LPS;group III lidocaine+LPS; group IV lidocaine.In group III, lidocaine was added to the cells30min after LPS.The cells were cultured for4h,12h,24h after LPS was added.Then TLR4and NF-kB protein was measured by Western Blot, TNF-a and IL-6was measured by ELISA.Results1. Western Blot showed control group alveolar type II epithelial cells have the expression of TLR4protein,but lower expression levels.LPS group cells TLR4and NF-kB protein expression was significantly higher than control group(P<0.05).L+LPS group compared with LPS group,TLR4and NF-kB protein expression were significantly increased at4h,12h,24h. control group, the alveolar type II epithelial cells the expression of TLR4and NF-kB protein volume compared with lidocaine group,no significant difference(P>0.05).2. ELISA showed LPS group alveolar type II epithelial cells the expression TNF-a and IL-6release amount compared with control group was significantly higher at each time point (P<0.05).In lidocaine+LPS group,TNF-a were significantly decreased compared with LPS group at each time point (P<0.05). There was no significant difference in TNF-a and IL-6release between control group and the lidocaine group(P>0.05).Conclusion1.TLR4may be mediated by the LPS induced alveolar type II epithelial cells in the inflammatory response.2. Lidocaine decreased LPS-induced alveolar type II epithelial cells inflammatory response which may be inhibited the activation of TLR4, Inhibiting the downstream transduction of NF-kB path,thereby reducing the inflammatory cytokines TNF-a and IL-6release. |