Objective To investigate the efficacy of erythropoietin (EPO) on cerebral ischemia of patients after intracranial aneurysm surgery.Methods Sixty patients with cerebral ischemia after operation of intracranial aneurysm,admitted to our hospital from May 2006 to August 2010,were randomly divided into control and treatment groups (n=30).Control group received conventional treatment,while the other group,on the basis of conventional therapy,was hypodermically given EPO at a dosage of 3000 IU for a consecutive 3 days.U.S.National Institutes of Health Stroke Scale (NIHSS) was used to score the patients on the admission day,1,2,3,4 and 5 weeks after EPO treatment; and diffusion-weighted imaging (DWI) of MRI was used in determining the changes of cerebral ischemic area on the ischemic day and l,2,3,4 and 5 weeks after ischemic.Results NIHSS scores of the EPO group (9.4±1.9,11.3±2.3,8.7±1.7) at 3,4 and 5 weeks after treatment were significantly higher as compared with those in the control group (10.8±2.2,7.9±1.6,10.1±2.3) (P＜0.05).Similarly,3,4 and 5 weeks after treatment,the reducing percentage of cerebral ischemia area in the EPO group (21.6±4.1,27.5±5.3,32.8±5.5)％ was larger than that in the control group (16.8±3.1,18.9±3.3,19.5±3.4)％ (P＜0.05).Conclusion EPO may play an effective role in cerebral ischemia of patients after intracranial aneurysm operation.

Objective To study the effect of electrical pre-stimulation of cerebellar fastigial nucleus (FN) on protein expression of telomerase reverse transcriptase (TERT) in rats with focal cerebral ischemia and reperfusion and its mechanism of mitochondrial protection. Methods Adult male Wistar rats (n=150) were randomly divided into a vehicle group (2-hcerebral ischemia,followed by 24,48 and 72 h of reperfusion) and a FN stimulation group (electrical stimulation of the FN for 1-h daily before 2-h cerebral ischemia,followed by 24,48 and 72 h of reperfusion).TTC staining was employed to measure ischemic lesion volumes.Western blotting was used to observe TERT and Bax protein expressions.The apoptotic cells were detected by TUNEL assay. Transmission electron microscopy was employed to detect the changes of mitochondrial ultrastructure. Results The size of the cerebral infarct in the vehicle group was significantly larger than that in the FN stimulation group at all reperfusion time points (P＜0.05).The relative value of TERT protein expression in the FN stimulation group (0.87±0.51,0.91 ±0.40 and 0.80±0.24) was also obviously higher than that in the vehicle group (0.73±0.37,0.80±0.51 and 0.64±0.33) at all reperfusion time points (P＜0.05); however, a significantly reduced number of TUNEL-positive cells in the FN stimulation group (53.60±5.18,64.00±2.37 and 49.83±4.26) was noted as compared with that in the vehicle group (63.57±3.74,75.40±5.55 and 60.00±2.37) at all reperfusion time points (P＜0.05).No significant difference on Bax protein expression was noted between the vehicle group and FN stimulation group (P＞0.05).The degree ofmitochondrial damage in the FN stimulation group (1.50±0.41,1.75±0.52 and 1.33±0.52) was also significantly lower than that in the vehicle group (2.50±0.63,3.08±0.58 and 2.33±0.41) at all reperfusion time points (P＜0.05). Conclusion TERT protein expression is significantly increased following FN stimulation, which can reduce ischcmic neuronal apoptosis by protecting the mitochondrial dysfunction.