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OBJECTIVE@#To discuss the mechanism of low molecular weight GTP binding protein RAC1 in the injury of neural function based on building the rat model of cerebral ischemia reperfusion.@*METHODS@#Middle cerebral artery of rats was ligated and the ligature was released to restore the perfusion after 2 h, the rat model of cerebral ischemia reperfusion injury was built, while the middle cerebral artery was ligated. The rats were randomly divided into the sham group, cerebral ischemia reperfusion group (I/R group) and the group with the injection of RAC1 activity inhibitor NSC23766 (NSC group). The survival and neurological severity score of rats in each group were observed and recorded. Nissl staining was employed to observe the nerve cells, and Western blot to detect expression of RAC1, superoxide dismutase and malondialdehyde.@*RESULTS@#Number of nerve cells for rats in NSC group was significantly more than that in I/R group, but significantly less than that in sham group, with the statistical difference (P < 0.05). The brain water content for rats in NSC group was significantly lower than that in I/R group, but significantly higher than that in sham group, with the statistical difference (P < 0.05). The expression of RAC1 and malondialdehyde for rats in NSC group was significantly lower than that in I/R group, but higher than that in sham group; while the expression of superoxide dismutase was lower than that in sham group, but higher than that in I/R group, with the statistical difference (P < 0.05).@*CONCLUSIONS@#The inhibition of RAC1 activity can reduce the oxidative stress, reduce the neurologic impairment because of cerebral ischemia reperfusion and thus protect the neural function.
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Objective To discuss the mechanism of low molecular weight GTP binding protein RAC1 in the injury of neural function based on building the rat model of cerebral ischemia reperfusion. Methods Middle cerebral artery of rats was ligated and the ligature was released to restore the perfusion after 2 h, the rat model of cerebral ischemia reperfusion injury was built, while the middle cerebral artery was ligated. The rats were randomly divided into the sham group, cerebral ischemia reperfusion group (I/R group) and the group with the injection of RAC1 activity inhibitor NSC23766 (NSC group). The survival and neurological severity score of rats in each group were observed and recorded. Nissl staining was employed to observe the nerve cells, and Western blot to detect expression of RAC1, superoxide dismutase and malondialdehyde. Results Number of nerve cells for rats in NSC group was significantly more than that in I/R group, but significantly less than that in sham group, with the statistical difference (P < 0.05). The brain water content for rats in NSC group was significantly lower than that in I/R group, but significantly higher than that in sham group, with the statistical difference (P < 0.05). The expression of RAC1 and malondialdehyde for rats in NSC group was significantly lower than that in I/R group, but higher than that in sham group; while the expression of superoxide dismutase was lower than that in sham group, but higher than that in I/R group, with the statistical difference (P < 0.05). Conclusions The inhibition of RAC1 activity can reduce the oxidative stress, reduce the neurologic impairment because of cerebral ischemia reperfusion and thus protect the neural function.
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Objective To explore the clinical features of sleep disorder in patients with stroke and its related factors. Methods Two hundred and four patients with stroke, admitted to our hospital from January 2005 to June 2010, were chosen; Pittsburgh Sleep Quality Index (PSQI) was employed to determine whether these patients had sleep disorder; the prevalences of sleep disorder in patients with different ages, genders and lesions of stroke were compared. Symptom Checklist-90 (SCL-90)questionnaire was used to compare the physical and mental conditions of patients with or without sleep disorder; Hamilton Depression Rating Scales (HAMD), Barthel index, and National Institutes of Health Stroke Scale (NIHSS) were employed to compare the differences of depression, viability and neurologic impairment in patients with or without sleep disorder. Results The prevalence of sleep disorder was 46.6% (95/204), and it was higher in female group (53.8% vs 38.8%; x2=3.851, P=0.033). Patients aged ≥70 years had the highest rate of sleep disorder (57.6%), followed by patients aged ＜50 years (41.5%),and then patients aged between 50 and 69 years showed the lowest rate (32.9%). The sites of stroke located in the subcortex, cortex, and cerebellum enjoyed their prevalences of 64.2%, 27.4% and 4.5%,respectively. The incidence of sleep disorder in patients with stroke located in the left hemisphere was obviously higher than that in the right hemisphere (x2=7.688, P=0.008). The results of 9 indexes of SCL-90, scores of HAMD and NIHSS in patients with sleep disorder were significantly higher than those in patients without sleep disorder, while the Barthel index was in the opposite position with obvious differences (P＜0.05). Conclusion High prevalence of sleep disorder in patients with stroke is noted,which is related to gender, age of the patients and the sites of stroke, and may lead to depression, anxiety,neurological functional deficit and decrease of life quality. And we should pay more attention to nursing care during all the treatment.