ABSTRACT
<p><b>OBJECTIVE</b>To investigate the expression and the subcellular localization of HDAC9 in different brain regions of mice after cerebral ischemic injury and explore the association between HDAC9 and ischemic stroke.</p><p><b>METHODS</b>Twenty-one male C57BL/6 mice were randomly divided into sham-operated group (n=9) and operated group (n=12). In the latter group, the mice with Zea-Longa neurological deficit scores of 2 or 3 following middle cerebral artery occlusion (MCAO) were assigned into MCAO group (n=9). Immunofluorescence was performed to investigate the subcellular localization of HDAC9 in the brain tissues on day 3 after MCAO. Western blotting and qRT-PCR were used to analyze the expression of HDAC9 in different regions of the brain. Results Immunofluorescence showed more intense HDAC9 expressions in the brain tissues around the infarct focus, and in the cells surrounding the infarct, HDAC9 expression was obviously increased in the cytoplasm and reduced in the cell nuclei. Compared with the other brain regions, the ipsilesional cortex with MCAO showed more abundant HDAC9 expressions at both the mRNA and protein levels (P<0.05).</p><p><b>CONCLUSION</b>HDAC9 may be closely related to cerebral ischemic injury and participate in the pathophysiological process of ischemic stroke.</p>
ABSTRACT
Objective To investigate the effect of electro-acupuncture (EA) on neurocan expression in the peri-infarct cortex in rats after middle cerebral artery occlusion (MCAO). Methods Ninety SD rats were randomly divided into sham-operated group (SO), MCAO group and EA treatment group (ET). Heat-coagulation method was used to establish MCAO in the rats in the latter two groups. The rats in the ET group received EA treatment at the acupoints Neiguan, Waiguan, Zusanli and Sanyinjiao for 1, 2, 3, or 4 weeks after MCAO. Immunohistochemistry, quantitative real-time RT-PCR and Western blotting were used to detect the expression of neurocan in the peri-infarct cortex after the treatment. Results Neurocan expression was detected in and around the GFAP-positive cells near the cerebral infarct foci following MCAO. Neurocan mRNA in rats with MCAO increased significantly 1 week after MCAO, reaching the peak level (0.806±0.224) in the second week and maintained the high expression level till 4 weeks after MCAO. In the EA treatment group, neurocan mRNA began to decrease in the first week of EA treatment followed by gradual decrease till reaching the lowest level (0.031± 0.018) in the 4th week of EA treatment. In the rats in MCAO group, the expression of neurocan protein increased progressively 1 week after MCAO and reached the highest level in the fourth week (0.878± 0.049); EA treatment significantly reduced neurocan expression in the second week of treatment, and resulted in the lowest expression level (0.292±0.042) in the fourth week of treatment. All these differences were statistically significant (P<0.05). Conclusions EA treatment can inhibit the expression of neurocan in the peri-infarct area, which might be one of the mechanisms of EA to reduce glial scar formation after cerebral infarction.
ABSTRACT
<p><b>OBJECTIVE</b>To explore the effect of leukoaraiosis on conscious disturbance in patients with acute cerebral infarction.</p><p><b>METHODS</b>A follow-up study including 138 patients with acute cerebral infarction matched with the diagnostic criteria of the Forth Cerebrovascular Disease Conference, were carried out. Patients were divided into two groups, using MRI to estimate the white substance process around cerebral ventricle, including 78 of them with leukoaraiosis and 60 without leukoaraiosis were followed up using Glasgow coma scale scores and England OCSP classification in 1 month, 3 month and 6 month after onset.</p><p><b>RESULTS</b>The independent factors of conscious disturbance included leukoaraiosis (OR = 5.294, 95% CI: 1.451-19.318), and OCSP classification (TACI and POCI especially) (OR = 14.489, 95% CI: 4.121-50.934). At the initial, the first month and the third month of the stroke episodes, significant difference (P < 0.05) was noticed when using Glasgow coma scales, and the scales in leukoaraiosis group was lower than the control.</p><p><b>CONCLUSION</b>TACI and POCI in OCSP classification were independent risk factors of conscious disturbance, and leukoaraiosis was also the independent factor. The incidence of conscious disturbance after stroke in patients with leukoaraiosis were lower than in that without leukoaraiosis. On the other hand, the degree of conscious disturbance was more serious and slower than those without leukoaraiosis, suggesting that the effect of leukoaraiosis was duplicate for conscious disturbance. Because patients with leukoraiosis had tolerance of chronic cerebral ischemia. The number of patients with conscious disturbance after stroke was fewer relatively. Leukoaraiosis had inactive effect for amelioration of conscious disturbance after three months of the episode. The grouping of OCSP played a primary while leukoaraiosis playing a secondary role, despite the patients with or without conscious disturbance after stroke.</p>