The Expression Of Notchl And NF-κB In The Experimental Intracerebral Hemorrhage In Rat Brain Tissue And The Intervention Of Statin

Objective:To explore the possible neuroprotection mechanism of statin after experimental intracerebral hemorrhage(ICH), we observe the expression level of Notchl and Nuclear factor-KB (NF-κB) in rats perihematomal brain tissue and the intervention effect of rosuvastatin to them, then we can provide a theoretical basis for statins therapy after ICH.Methodes:The one hundred and twenty Spragne Dawley(SD) rats were randomly selected and divided into shamed-operation group(group A, forty rats) and ICH modle group(eighty rats).we injected fresh non-heparin autologous arterial blood into the adult SD rats right basal ganglia(the caudate nucleus) by stereotactic apparatus to build up rats experimental ICH modle, the group A injected the same amount of sterile saline in the same way. Then we randomly divided ICH modle group into ICH group(group B, forty rats) and rosuvastatin intervention group(group C, forty rats), the group C rats were given rosuvastatin(10mg/kg-d) administer by gavage. While the group A and B rats were given the same dose saline at the time. After injecting, using Garcia score to assessed the neurological deficit of each group(group A,B and C) at every time point(24h,72h,5d,7d) after ICH; Then the SD rats were killed, and using immunohistochemistry and Western Blot method to measure each group and each time point the expression level of Notchl and NF-κB P65in the perihematoma.Results:The Garcia score results show that, compared with the same time of the shamed-operation group (group A), intracerebral hemorrhage model group (group B) neurological score was significantly lower, the difference was statistically significant (P<0.05); Compared with the same time of group A, rosuvastatin intervention group (group C) at24h,72h and5d have lower score, the difference was statistically significant (P<0.05);But at7d, the neurological function of group C was restored, there is no significant difference (P>0.05) compared with group A; Compared with group B at each time point, the neurological deficit score were increased, the difference was statistically significant (P<0.05).Immunohistochemistry results showed that the shamed-operation group (group A) had a small amount of Notchl and NF-κB P65-positive cells at each time point, but no significant difference (P>0.05) between them; Intracerebral hemorrhage model group (group B) and rosuvastatin intervention group (group C) at each time point compared with the corresponding time points in group A, Notchl and NF-κB P65positive cells was significantly increased, and the difference was statistically significant (P<0.01); Group C compared with group B at each time points, Notchl and NF-κB P65positive cells decreased significantly (P <0.05).Western Blot results showed that the shamed-operation group(group A) had small amount of Notchl and NF-κB P65protein expression, but the protein levels of each time point were same; At each time points of intracerebral hemorrhage model group (group B), the Notchl and NF-κB P65protein expression was significantly increased; The expression level of Notchl and NF-κB P65protein in rosuvastatin intervention group (group C) were weaker compared with group B.Conclusions:Rosuvastatin can relieve neurological function deficit in rats with experimental intracerebral hemorrhage; Rosuvastatin may can inhibit inflammation and reduce brain injury to play its neuroprotective effect by reducing the expression of Notch1and NF-κB P65at experimental ICH perihematomal brain tissue of rats.