The effect of propofol on the expression of nuclear factor-kappa B and the ultrastructure after intracerebral hemorrhage in rats

Objective To investigate the effect of propofol on expression of nuclear factor-kappa B(NF-κB) and the ultrastructure after intracerebral hemorrhage(ICH) in rats.Methods Sixty-five male adult Sprague-Dawley rats were randomly divided into normal group(n=5),sham-operation group(n=25),model group(n=25) and treatment group(n=10). The sham-operation and model groups were redivided into 5 subgroups(6,12 h,1,2,and 4 days) according to the time that the rats were sacrificed;the treatment group were redivided into 2 subgroups(1 and 2 days).The model and treatment groups used a model of ICH induced by collagenase Ⅶ injection by stereotatic technique,and the sham-operation group used isotonic saline solution instead;the rats in the treatment group were injected propofol 100 mg/kg IP once a day,and the rats in the sham-operation and model groups were injected isotonic saline solution instead.The dynamic changes of the expression of NFκB in the cerebral tissues surrounding the hematoma were assayed by Western blot.The ultrastructural changes of neurocytes surrounding the hematoma 2 days after the operation were observed with a transmission electron microscope.Results The expression of NF-κB increased significantly at 12 hours after ICH(P0.05).It reached maximum at 1 day(P0.01),and began to decrease at 2 days(P0.01),and continued to express at 4 days(P0.05).The neuronal injury was obvious 2 days after ICH under transmission electron microscope.The expressions of NF-κB(grey scale values) at 1 and 2 days in the treatment group were 61±19 and 24±6,respectively,and they were significantly lower than 92±16 and 65±13 in the model group(P0.05).The ultrastructural changes in neurons were also less severe than those in the model group.Conclusions Inflammatory reaction was involved in brain tissues surrounding hematoma after ICH.Propofol may effectively reduce the inflammatory reaction after ICH and protect the neuronal structures.Its mechanism may be associated with the inhibition of the expression of NF-κB.