Expressions of complement 9 and nuclear factor-kappa B65 in perihematomal tissue following intra cerebral hemorrhage in rats and the interventional effect of astragalus polysaccharides

Objective To discuss the expressions of complement (C9) and nuclear factor-kappa B (NF-κB65) in perihematomal tissue following experimental intracerebral hemorrhage (ICH) in rats and the effect of astragalus polysaccharides (APS) intervention on them. Methods Sixty-nine male SD rats were randomly allocated into sham-operation, model, and treatment groups(n=23 in each group). They were redivided into 6 hour, 1, 3, and 5 day subgroups according to the time of sacrifice of animals. Five rats in each subgroup were selected for immunohistochemical staining at each time point. Three rats were select for transmission electron microscope examination at the 3 day time point. ICH model was induced by collagenase Ⅶ in the model group and treatment group. The collagenase Ⅶ were replaced with an equal volume of isotonic saline solution in the sham-operation group. Two hours after procedures, APS 2 mL ( 25 mg/kg ) was administered intraperitoneally once a day in the treatment group. The neurological behavioral scores in rats were evaluated at 6 hour, 1, 3, and 5 day intervals. The changes of C9 and NF-κB65 expressions in perihematomal tissue at different time intervals were detected with immunohistochemical method. The ultrastructure changes of perihematomal neurons were observed with transmission electron microscope 3 days after the procedures. Results C9 began to express 6 hours after ICH and reached a peak at 24 hours in the model group and treatment group; NF-κB65 began to express at 6 hours and reached a peak at 3 days. The expressions at all time intervals in both groups were higher than those in the control group (P0.05-0.01). The expression of NF-κB65 was positively correlated that of C9 (r=0.752, P0.05). The neurological behavior scores of the rats in the treatment group decreased significantly at 3 and 5 days ( P0.05 ) as compared with the model group, and the changed neuronal ultrastructure was also milder than the model group. Conclusion C9 and NF-κB65 participate in neuronal injury after ICH; it may exert its neuroprotective effect by inhibiting the expressions of C9 and NF-κB65 after the intervention of astragalus polysaccharides.