RESUMO
Objective To observe the influence of Hemin on both the expression of neuroglobin (Ngb) and Tau protein phosphorylation in rats with vascular dementia (VD),and explore the effect and mechanism of Ngb in VD. Methods VD model was established in rats with a permanent bilateral common carotid arteries occlusion(2-VO). Fifty four healthy male SD rats were randomly divided into 3 groups:sham operation group,VD group and Hemin group. According to ischemic time,the animals in each group were randomly allocated into 1 week subgroup,4 weeks subgroup and 8 weeks subgroup(n=6 in each subgroup). The learning and memory ability of rats were evaluated by Morris water maze test. The brain histopathological changes were observed by HE staining and the expression of Ngb and phosphorylated Tau ( p-Tau) was de-termined by Western blot. Results Compared with the sham operation group,after 2-VO the escape latency extended (all P<0. 05) and cross-platform performance reduced in rats in both VD group and Hemin group (all P<0. 05). The learning and memory ability of rats in Hemin group was better than that in VD group at the corresponding time point:the increase in the number of crossing platforms(1 week:Hemin group (7. 00± 0. 89) times vs VD group (5. 50±1. 22) times,t=2. 42,P<0. 05;4 weeks:Hemin group (5. 33±0. 52) times vs VD group (3. 50±1. 04) times,t=3. 84,P<0. 01;8 weeks:Hemin group (6. 50±0. 55) times vs VD group (4. 50±1. 05) times,t=4. 14,P<0. 01). The expression of Ngb and phosphorylated Tau (p-Tau) increased in VD group and Hemin group (P<0. 01). Compared with VD group,the expression of Ngb in Hemin group was increased(1 week:Hemin group (3. 45±0. 23) vs VD group (2. 56±0. 08),t=5. 67,P<0. 01;4 weeks:Hemin group (3. 08±0. 13) vs VD group (2. 28±0. 08),t=7. 96,P<0. 01;8 weeks:Hemin group (2. 82± 0. 12) vs VD group (2. 05±0. 10),t=7. 28,P<0. 01),while p-Tau was decreased (1 week:Hemin group (1. 57±0. 12) vs VD group (2. 40±0. 15),t=7. 62,P<0. 01;4 weeks:Hemin group ( 2. 14±0. 21) vs VD group (3. 18±0. 14),t=8. 23,P<0. 01;8 weeks:Hemin group (1. 83±0. 13) vs VD group (2. 79±0. 19), t=4. 91,P<0. 01). In VD group and Hemin group,the learning and memory ability exhibited a negative cor-relation with Ngb (r=-0. 892,P<0. 01),whereas a positive correlation with p-Tau (r=0. 932,P<0. 01). Conclusion Hemin induces high expression of Ngb and inhibits Tau phosphorylation in VD rats. Ngb may play a neuroprotective role in the development of VD by regulating Tau phosphorylation.
RESUMO
Objective To investigate the serum asymmetric dimethylarginine (ADMA)expression in patients with acute cerebral infarction. Methods A total of 100 patients with acute cerebral infarction admitted to the Department of Neurology,the First Affiliated Hospital of Xi′an Medical College from March 2013 to August 2015 were enrolled retrospectively. According to the National Institutes of Health Stroke Scale (NIHSS)scores,they were divided into three groups:mild infarction (n =21; 15);100 healthy subjects without cerebrovascular disease in the same period were used as a control group. Enzyme linked immunosorbent assay was used to detect the plasma ADMA concentration,and the levels of plasma ADMA among the groups were compared. Results The concentrations of plasma ADMA of the mild,moderate,severe cerebral infarction,and the control groups were 0. 80 ± 0. 16,1. 14 ± 0. 28,1. 33 ± 0. 33,and 0. 52 ± 0. 16 μmol/ L,respectively. There were significant differences among the groups (F = 2. 32,P < 0. 05). Multivariate logistic regression analysis suggested that ADMA was an independent risk factor for cerebral infarction (OR,1. 140,95% CI 1. 078 -1. 212,P = 0. 045). Conclusions The expression levels of plasma ADMA increased gradually in patients with mild,moderate,and severe cerebral infarction. The higher the ADMA levels,the severe the neurological deficit would be. ADMA might be an independent risk factor for cerebral infarction.