Observation On The Influence Of Erigeron On Hemorrhagic Brain Injury In Rats

Objective To explore the protective effect of breviscapine injection on hemorrhagicbrain injury in rats.Method144healthy SD rats were randomly divided into blank control group, shamoperative group, cerebral hemorrhage model group and breviscapus treatment group. Cerebralhemorrhage model was established in rats with a mixture of collagenase and heparin injectedinto caudate-putamen, and cerebral hemorrhage model group and breviscapus treatment groupwere all killed on3rd,5th, and7th day after drug injection. The neurological functional scoresof each group were evaluated according to the Berdson Scoring Criteria. The expression levelsof inflammatory cytokines,TNF-and IL-8, were tested by enzyme linked immunosorbentassay (ELISA), apoptotic cells were detected by TUNEL fluorescence method, apoptosis rateof nerve cells was determined by flow cytometry. The expression of bcl-2and bax aroundhemorrhagic focus was tested by immunohistochemical methods.Results1.Hemiplegic symptom appeared in cerebral hemorrhage model group andbreviscapus treatment group at each time point. Comparing breviscapus treatment group withcerebral hemorrhage model group at the same time point, neurological score of breviscapustreated rats was significantly lower, there was statistical significance (P <0.01).2.Inflammatory cytokines in plasma were tested by enzyme-linked immunosorbent assay,which showed that TNF-α and IL-8were significantly increased in the cerebral hemorrhagemodel group at each time point by comparison to blank control group. There was statisticalsignificance between these two groups (P <0.01). Inflammatory cytokines TNF-α and IL-8inplasma of breviscapine treatment group were significantly decreased at each time point, compared with cerebral hemorrhage model group at the same time point, the difference wasstatistically significant (P <0.01).3.In NeuN/TUNEL florescence staining, perihematomalcells exhibitted nucleolus pyknosis and margination, which suggested that perihematomalTUNEL-positive cells were decreased significantly in the breviscapine treatment group at eachtime point, compared with brain hemorrhage model group at the same time point, thedifference was statistically significant (P <0.01).4.The apoptosis rate of perihematomal braincells were tested by flow cytometry analysis and showed that brain cells apoptosis of cerebralperihematomal in breviscapine treatment group at each time point reducedsignificantly,compared with brain hemorrhage model group at the same time point, thedifference was statistically significant (P <0.01).5.Immunohistochemical detection showedthat perihematomal bcl-2-positive cells in breviscapine treatment group at each time pointincreased significantly, compared with cerebral hemorrhage model group, the difference wasstatistically significant (P <0.01), while bax-positive cells were significantly decreased, so theratio of bcl-2/bax increased. The difference was statistically significant (P <0.01).Conclusions a. Breviscapine can significantly reduce nerve function scores of the ratswith intracerebral hemorrhage and promote the recovery of the neurological function of ratswith intracerebral hemorrhage. b. Breviscapine can reduce the expression of inflammatorycytokines TNF-α and IL-8in rats’ plasma with cerebral hemorrhage and inhibit theinflammatory response in the perihematomal tissues. c. Breviscapine can reduce the numberof perihematomal TUNEL-positive cells and apoptosis rate of perihematomal cells in rats bypromoting the expression of bcl-2protein.d.Breviscapine may inhibit the expression of baxand increase the ratio of bcl-2/bax,therefor further to inhibit perihematomal cellsapoptosis.