The improving brain circulation is the most important aspect in protecting brain from the ischemic trauma. This frauma on pathophysiology includes the two stages which are related to different treatments. The paper induced some therapeutic progress, such as thrombolytic therapy, the use of anticoagulation agents, antiplatelet drugs, neuroprotectine agents, intracerebral transplantation, antiedama, and reducing intracranieal pressure.

Objective To study the expression of hemeoxygenase-1 (HO-1) and change of superoxide dismutase (SOD) activity in perihematoma after intracerebral hemorrhage (ICH). Methods The rats were randomly divided into sham operating group and intracerebral hemorrhage group.Rat ICH models were induced using stereotactic infusion autologous blood 50 ?l into the caudate nucleus. At the due time, the rats were killed and brain tissues were removed for detection of HO-1 and measurement of SOD by immunohistochemical and xanthine hydrocarbonylation methods. Results Following ICH, few HO-1 positive cells were observed in brain tissue perihemota at 6 h, peaked at 48 h ( P0.05), then decreased gradually and reached the minimum at 72 h ( P0.05). The change of SOD in brain tissue perihematoma was negatively correlated with the expression of HO-1 (r=-0.878, P

Objective To investigate the correlation between the expression of redox factor-1 (Ref-1) and neuronal apoptosis around hematoma after experimental intracerebral hemorrhage (ICH) in rats.Methods ICH model of rat was induced using stereotactic infusion antilogous blood 50 ?l into the caudate nucleus. The male animals were randomly divided into sham operation group, normal control group and hemorrhage group. TUNEL and immunohistochemistry methods were used to detect apoptosis and the expression of Ref-1 in cerebral tissues at different time, respectively.Results The expression of Ref-1 was negatively correlated with neuronal apoptosis around hematoma after ICH (r=-0.745, P

Objective To investigate the expression of IGF-1 in cerebral tisse,and its correlation with Glutamate expression and neuronal apoptosis,and to study the role of IGF-1 in the pathophysiologie process of ICH.Methods ICH model was induced in rats by infusing 50?l autologous blood into the eaudate nucleus with stereotaetie device.The animals were randomly divided into sham-operation group,ICH group and exogenous IGF-1 intervention group.Every rat was killed and brain tissue was collected.Immunohistoehemitry assay was used to detect the expression of IGF-1 and Glutamate,and TUNEL method used to detect apoptosis in cerebral tissues.Result At 2 hours after ICH,IGF-1 positive cells appeared around the hematoma in the brain,peaked after 24 hours,and returned to normal level on the 7th day. Glutamate positive cells appeared around the hematoma at 2 hours,peaked on the 3rd day,and its high level expression lasted to the 7th day.TUNEL- positive cells appeared at 8 hours,peaked on the 3rd day,and few apoptotic ceils could be found on the 7th day.The expression of IGF-1 was positively correlated with apoptotie cells and the expression of Glutamate.The amounts of Glutamate positive cells and TUNEL positive cells were significantly reduced after intervention with exogenous IGF-1.Conclusion IGF-1 participated in the pathophysiologic course of ICH.IGF-1 repaired and protected the brain tissue from damage after ICH.

Objective To investigate the changes and correlation between nuclear factor-?B (NF-?B) expression and brain water content (BWC) in perihematoma after experimental intracerebral hemorrhage (ICH) in rats. Methods Experimental ICH models of rat were made by injecting autologous blood using stereotaxic method. The expression of NF-?B in cerebral tissues was detected by immunohistochemistry technique. At the due time, BWC was measurement by day-wet method.Results NF-?B expression increased obviously at 6 h and peaked at 48 h in ICH group(P

Objective To study the effect of mild hypothermia on neuronal apoptosis and Bcl 2,Bax during cerebral ischemia in middle cerebral artery occlusions(MCAO) in rats.Methods The model of MCAO was set up in rats using the Longa's way,and mild hypothermia was treated for 0.5h,1h,3h. After reperfusion(24h) the rat brains were cut into three sections for TUNEL staining and Bcl 2?Bax protein immunohistochemical staining.Results 1)The numbers of apoptotic cells and Bax cells in the mild hypothermia group(1h, 3h) decreased remarkable as compared with the control group( P

Objective To study the correlation between the expression of intercellular adhesion molecule 1(ICAM 1) and leukocyte infiltration, and explore the effects of mild hypothermia.Methods ICAM 1 positive expression and leukocyte infiltration in the ischemic regions were determined using immunohistochemitry and histological HE staining techniques at different reperfusion time(2 h,8 h,24 h,48 h and 72 h) after middle cerebral artery occlusion (MCAO) for 3h in rats, and mild hypothermia was given after MCAO followed by 24h reperfusion.Results (1)The expression of ICAM 1 raised obviously 2h after cerebral ischemia reperfusion, and peaked at 24h ( P

Objective To study the effect of zVADfmk(a Caspase inhibitor) on Caspase-3 activation and neuronal apoptosis after intracerebral hemorrhage (ICH) in rats.Methods ICH model was made by stereotactic infusing 50?l autologous blood into the caudate nucleus. zVADfmk was given via intraventricular injection. TUNEL staining and immunohistochemitry method were used to detect the expression of apoptosis and Caspase-3 in cerebral tissues at different time point.Results After ICH, Caspase-3 and TUNEL positive cells increased obviously in the perihematomal brain edema zone compared with the pseudo-operation group ( P

Statins can substantially lower the incidence of cerebral ischemia and attenuate cerebral ischemic injury. Statins may exert their protective effects via different mechanisms, including stabilizing atherosclerotic plaques, improving endothelial function, reducing inflammatory reaction and reperfusion injury. Moreover, they may also reduce the occurrence of dementia by preventing ?-amyloid from formation and reducing secretion of apolipoprotein E.

Objective To investigate the effect of human telomerase reverse transcriptase C27 polypeptide (hTERTC27) over-expression on orthotopic implanted tumor growth which induced by nasopharyngeal carcinoma cells C666-1 in vivo.Methods Stably transfected C666-1 cell lines were used to establish subcutaneously transplanted tumor mouse model.The tumor growth was observed and the tumor growth curve was made by measuring the volumes of tumors every day.HE staining was used to observe the change of histomorphology.The expressions of cleaved Caspase-3,Caspase-9,PARP,bax and bcl-2 were detected by Western blot analysis.Results The in vivo mouse model showed that over-expression of hTERTC27 significantly reduced tumor volume and tumor weight (P ＜ 0.05),and decreased the local muscle infiltration.Over-expression of hTERTC27 significantly up-regulated the expressions of cleaved Caspase-3,Caspase-9,PARP and bax (P ＜ 0.01),and down-regulated the expression of bcl-2 (P ＜ 0.01).Conclusion The results indicate that over-expression of hTERTC27 can obviously inhibit the growth of transplanted tumor in nude mice,which is possibly related to the regulation of bax and bcl-2 expression.