Purpose To investigate the effect of desflurane preconditioning on nuclear factor-κB (NF-κB) activation induced by anoxia / reoxygenation (A/R) injury in ECV304 cells in vitro. Methods Cell line was used. In Part A experiment, the ECV304 cells were divided into 6 groups: the control group and the other five groups stimulated by TNF-α with different duration. The protein levels of IκB-α (the inhibitory factor of the NF-κB) and its phosphorylation form, D-IκB-α, were detected by Western blot method. In Part B experiment, the ECV-304 cells were divided into 5 groups, group I: control; group II: A/R ; group III : A/R+ TNF-α 10 ng/mL; group IV : desflurane 1. 0 MAC precon-ditioning+ A/R; group V: desflurane 1. 0 MAC preconditioning+ A/R+ TNF-α 10 ng/mL. Then, the intracellular localization of NF-κB/ p65 was analyzed by indirect immumofluorescence method. Results Degradation of IκB-α reached its peak 30 min after TNF-α stimulation, while the phosphorylation activation of IκB-α-(p- IκB-α) did so 1 h after stimulation. In TNF-α stimulated cells, NF-κB/ p65 nucleus translocation , which is the indication of NF-κB activation, was significantly inhibited by preconditioning with 1.0MAC desflurane. Conclusions The inhibition of NF-κB activation could be one of the protective mechanisms for the desflurane preconditioning against A/R injury.
|Number of pages||5|
|Journal||Fudan University Journal of Medical Sciences|
|Publication status||Published - Nov 2007|