The Experimental Studies On The Brain Protective Effects And Mechanisms Of Edaravone On The Intracerebral Hemorrhage Injury Of Rat

Part one: Effect of edaravone on cerebral edema and lipid peroxidation in rat brain after intracerebral hemorrhageObjective To explore the protective effect of edaravone on oxidation damage after intracerebral hemorrhage(ICH ).Methods In this study,105 SD rats were included and were divided into edaravone treating group(n=35)and lCH control group(n=35)and sham operation group(n=35).We induced intracerebral hemorrhage in rats with injecting autologous blood into the right caudate. Water content in perihematoma was examined with wet dry weight measurements. Theactivity of superoxide dismutase (SOD)and the contents of malondialdehyde (MDA)in perihematoma were detected with spectrophotometry. Results The activity of SOD at various stages of post operation in ICH control group was lower than that in sham operation group(P<0.05)and the content of MDA at various stages of post operation in ICH control group was higher than those in sham operation group(P<0.05). Water contents at various stages of post operation in ICH control group were significantly positively correlated with the content of MDA (r=0.654,P<0.01),while they were significantly negatively correlated with the activity of SOD (r=-0.631,P<0.01).Compared with ICH control group, the content of MDA at 12-96h in Edaravone treating group was significantly decreased(P<0.05)and the activity of SOD at l2-120h in Edaravone treating group was significantly increased(P<0.05).Water contents at various stages of post operation in Edaravone treating group were significantly positively correlated with the content of MDA (r=0.418,P<0.05),while they were significantly negatively correlated with the level of SOD (r=-0.462,P<0.05).Conclusions The rats with lCH showed significant oxidation damage in perihematoma,which may be associated with brain edema.Treatment with Edaravone in a rat model of intracerebral hrmorrhage reduced obviously oxidation damage. The new anti-free radicals drug may play an important role in treating brain edema after intracerebral hemorrhage. Part two: The effects of edaravone on cell Apoptosis and expression of Bcl-2 and Bax,NF-κB protein in intracerebral hemorrhage RatObjective To study effect of edaravone on cell apoptosis and expression of Bcl-2,Bax,NF-κB protein following intracerebral hemorrhage in rats and explore the protective effect of edaravone on brain damage. Methods In this study,36 SD rats were included and were divided into edaravone treating group, ICH control group and sham operation group(n=12,respectively).We induced intracerebral hemorrhage in rats with injecting autologous blood into the right caudate. The contents of MDA in perihematoma were detected with spectrophotometry. Apoptotic was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) method. Expression of anti-apoptotic protein Bcl-2 , pro-apoptotic protein Bax and NF-κB in cardiac myocytes was detected by immunohistochemistry method. Results compared with sham operation group, the content of MDA, the apoptotic cells and the expression of Bcl-2 and Bax protein were increased significantly in ICH group;while compared with ICH group, the content of MDA, the apoptotic cells and the expression of Bax protein were decreased obviously and the expression of Bcl-2 protein was upregulated in edaravone treating group. Conclusion These results demonstrate that edaravone can inhibit brain cell apoptosis.it maybe via alleviate oxidative stress and upregulating Bcl-2 and downregulating Bax,NF-κB proteins.