Transplanted bone marrow stromal cells improve cognitive dysfunction due to aging hypoperfusion in rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Aging is an important risk factor for vascular dementia, and D-galactose (D-gal) injection can simulate the pathology of aging. Two-vessel occlusion of common carotid arteries (2VO) is the most popular model for vascular dementia. This study was aimed to investigate the possibility of D-gal injection plus 2VO simulating cognitive impairment of aging vascular dementia; and whether transplanted bone marrow stromal cells (BMSCs) can improve the cognitive function induced by D-gal injection plus 2VO.</p><p><b>METHODS</b>Totally 30 male Sprague-Dawley rats were divided into 5 groups equivalently: control group, D-gal group, D-gal + 2VO group, D-gal + 2VO + saline water group, and D-gal + 2VO + BMSCs group. Aging hypoperfusion rats were created by subcutaneous injection of D-gal and occlusion of two common carotid arteries. BMSCs or saline water was stereotactically transplanted into the subventricular zone as treatment vehicles at 24 hours post operation. Two-way repeat analysis of variance (ANOVA) was used for significance analysis of 5 groups at 6 weeks post transplantation; moreover, Tamhane's test (equal variance not assumed) and least significant difference (LSD) test (equal variance assumed) were used for pairwise comparison in Morris water maze (MWM).</p><p><b>RESULTS</b>Transplanted BMSCs distributed around the lateral ventricles and acquired the phenotypes of neurons and astrocytes. In terms of swimming path distance and escape latency in MWM, D-gal + 2VO + BMSC group showed significant improvement than the D-gal + 2VO group but was still obviously worse than the control group (both P < 0.05). There was no significant difference in swimming speed for all 5 groups.</p><p><b>CONCLUSIONS</b>D-gal plus 2VO induces cognitive dysfunction. The engrafted BMSCs exhibit the beneficial effect on cognitive function via promotion interactively with host brain.</p>

Effects of L-lysine monohydrochloride on insulin and blood glucose levels in spinal cord injured rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Hyperglycemia in brain and spinal cord could aggravate neurologic impairment. Recent studies showed that L-lysine monohydrochloride (LMH) could increase the insulin secretion and regulate the blood glucose level. The aim of the present study was to investigate the effects of LMH on pancreatic islet B cells, the levels of endogenous insulin and blood glucose in spinal cord injured rats.</p><p><b>METHODS</b>Forty male Wistar rats were divided into four groups, namely, normal control group, model group, high-dose LMH group (621.5 mg/kg equal to LMH 1/8 LD50), and low-dose LMH group (310.8 mg/kg equal to LMH 1/16 LD50). The model of spinal cord injured rat was established by hemi-transection at the lower right thoracic spinal cord. LMH was administered via intraperitoneal injection once spinal cord injury was produced in rats. All rats were sacrificed 48 hours after spinal cord injured. The effects of LMH on pancreatic islet B cells, the content of endogenous insulin, and the level of blood glucose were observed with immunohistochemical method, radioimmunoassay method, and biochemical analyzer, respectively.</p><p><b>RESULTS</b>The insulin immunohistochemical intensities of islet B cells were significantly weaker in model group than those in normal control group (P < 0.01). The levels of endogenous insulin were significantly lower and the blood glucose levels were significantly higher in model group than those in normal control group (P < 0.01). The insulin immunohistochemical intensities of islet B cells were significantly stronger in high-dose LMH group than those in model group (P < 0.05). In addition, we found that the levels of endogenous insulin were significantly higher and the blood glucose levels were significantly lower in high-dose LMH group than those in model group (P < 0.05). There were no significant differences in the insulin immunohistochemical intensities of islet B cells, the levels of endogenous insulin and the blood glucose between low-dose LMH group and model group (P > 0.05).</p><p><b>CONCLUSION</b>LMH, but dose-dependent, might participate in the regulation of pancreatic islet B cells, and then reduce the blood glucose levels in the spinal cord injured rats.</p>

Unilateral amyloid-beta25-35 injection into the rat amygdala increases the expressions of aberrant tau phosphorylation kinases / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Neuropathologically, Alzheimer disease (AD) is characterized by the presence of extracellular plaques enriched in beta-amyloid peptides; however, the mechanism by which it results in the neurotoxicity is uncertain. The purpose of this study was to investigate whether it would prompt the progress of Alzheimer disease via enhancement of aberrant phosphorylated tau that results from its increased kinase gene expression.</p><p><b>METHODS</b>Twenty-four male rats were divided into three groups, and each group had 8 rats: control, sham-operated, and Abeta(25-35) injected AD model groups. AD rat models were created by unilateral injections of Abeta(25-35) into the amygdala. The hyperphosphorylated tau protein was estimated by immunohistochemistry with paired helical filament-1 (PHF-1) antibody and paired helical filament-tau (AT8) antibody. The expressions of glycogen synthase kinase-3beta (GSK-3beta) and p38 mitogen-activated protein kinase (P(38)MAPK) mRNA were observed by in situ hybridization.</p><p><b>RESULTS</b>Compared with the control and sham-operated groups, the evaluation of paired AT8 and paired helical filament-1 (PHF-1) in the cortexes and hippocampus of the AD model group showed the numbers of AT8 and PHF-1 positive cells, as well as the optical density (OD) values of the proteins were significantly higher (AT8: in CA2: 0.318 +/- 0.037 vs. 0.135 +/- 0.028, 0.136 +/- 0.031; in frontal cortex: 0.278 +/- 0.040 vs. 0.130 +/- 0.028, 0.190 +/- 0.037. PHF-1: in CA2: 0.386 +/- 0.034 vs. 0.139 +/- 0.010, 0.193 +/- 0.041; in frontal cortex: 0.395 +/- 0.050 vs. 0.159 +/- 0.030, 0.190 +/- 0.044, respectively, P < 0.01); the number of GSK-3beta mRNA and P(38)MAPK mRNA positive cells of the AD model group, as well as the OD values, also increased significantly in the cortexes, hippocampus (GSK-3beta-mRNA: in CA2: 0.384 +/- 0.012 vs. 0.190 +/- 0.015, 0.258 +/- 0.064; in frontal cortex: 0.398 +/- 0.018 vs. 0.184 +/- 0.031, 0.218 +/- 0.049. P(38)MAPK mRNA: in CA2: 0.409 +/- 0.038 vs. 0.161 +/- 0.041, 0.189 +/- 0.035; in frontal cortex: 0.423 +/- 0.070 vs. 0.160 +/- 0.032, 0.203 +/- 0.053, respectively, P < 0.01).</p><p><b>CONCLUSION</b>Unilateral injection of Abeta(25-35) into the rat amygdala increases the generation of aberrant phosphorylated tau by increasing GSK-3beta and P(38)MAPK gene expression, that accelerates the process of Alzhemer's disease.</p>

A clinical study of low frequency electric stimulation on the patients with vertebrobasUar insufficiency / 中华物理医学与康复杂志

Objective To explore the effects of low frequency electric stimulation on the clinical manifes- tation and its influence on the level of plasma Endothelin (ET),atrial natriuretic peptide (ANP),thromboxane B_2 (TXB_2),angiotensinⅡ(AngⅡ),Calcitonin Gene Related Peptide(CGRP) and Neuron-specific Enolase(NSE) and its clinical significance in the patients with vertebrobasilar insufficiency(VBI). Methods One hundred and tewenty cases of VBI patients were randomly divided into two groups:a treatment group and a control group.Both groups received routine drug treatment.The treatment group (n=60) was also treated with low frequency electric stimulation at bilateral mastoid processfes in addition.The improved rate of the clinical symptom,the plasma level of ET,ANP,TXB_2,AngⅡ,GRP and NSE were observed after treatment. Results The patients treated in the treatment group had significantly better outcome than the control group in terms of symptom relief.The effective rate was 87.93% and 67.80% in the treatment group and control group,respectively(P

Clinical significance of dynamic changes of plasma neuron-specific enolase,endothelin and calcitonin gene-related peptide in elderly patients with acute cerebral infarction / 中华老年医学杂志

Objective To investigate the dynamic changes of serum levels of neuron-specific enolase(NSE),endothelin(ET)and calcitonin gene-related peptide(CGRP)and their clinical significance in the elderly patients with acute cerebral infarction.Methods One hundred and twenty elderly patients with acute cerebral infarction(ACI),60 elderly patients with lacunar infarct,60 elderly patients with hypertension and 60 elderly patients with cerebral artherosclerosis were enrolled. The areas of infarction were measured and the venous blood samples at different times were collected after cerebral infarction to determine the concentrations of NSE,ET and CGRP by radioimmunoassay. Results There were dynamic changes of the plasma levels of NSE,ET and CGRP.In the early time the plasma levels of NSE and ET of the elderly patients with acute cerebral infarction were significantly higher than those of the elderly patients with cerebral artherosclerosis,or with hypertension,or with lacunar infarct(P＜0.01,P＜0.01,P＜0.05,respectively),and were gradually declined along with timing.In ACI group,the level of NSE began to increase gradually after 24 hours,reached the highest in 2 days,and decreased to normal after 14 days,but the level of ET was always higher than those in the cerebral artherosclerosis and hypertension groups.The ET levels in lacunar infarct and hypertension groups were also significantly higher than in the cerebral artherosclerosis group(P＜0.01).However,when compared with the cerebral artherosclerosis and hypertension groups,the plasma concentrations of CGRP in cerebral infarction and lacunar infarct groups were obviously lower(P＜0.01),and increased gradually.We also found the larger the infarction area,the lower the level of CGRP.Conclusions The NSE,ET and CGRP concentrations are associated closely with acute cerebral infaction.Monitoring the level of NSE is applicable for early diagnosis of cerebral infarction.