In vivo transplantation of bone marrow mesenchymal stem cells accelerates repair of injured gastric mucosa in rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Adult stem cells provide a promising alternative for the treatment of injured tissues. We aimed to investigate the effect of in vivo transplantation of bone marrow mesenchymal stem cells (BMMSCs) on injured gastric mucosa in rats.</p><p><b>METHODS</b>The gastric ulcer in rats was induced by indomethacin. BMMSCs from male rats, labeled with the fluorescent cell linker 5,6-carboxyfluorescein diacetate succinimidyl ester (CFDA SE), were transplanted into the female rats via tail vein injection. The healing process of gastric ulcers was monitored by HE staining. The protein levels of vascular endothelial growth factor (VEGF) and the epidermal growth factor receptor (EGFR) in the injured gastric mucosa were determined by immunohistochemistry.</p><p><b>RESULTS</b>At 48 and 72 hours after BMMSCs transplantation, the CFDA SE labeled cells were found scattered in the injured gastric mucosa, but not in the gastric mucosa of control rats. At 72 hours after BMMSCs transplantation, the mean ulcer index was 12.67 ± 2.16 in the BMMSCs transplanted group and 17.33 ± 1.97 in vehicle-treated controls (P < 0.01). Both VEGF and EGFR protein expression levels were significantly higher in the gastric section from the rats that received BMMSCs transplantation as compared to rats without BMMSCs transplantation.</p><p><b>CONCLUSION</b>Autologous BMMSCs transplantation can accelerate gastric ulcer healing in injured gastric mucosa in a rodent model.</p>

Effect of Shuyusan on neuropeptide Y and serotonin expression in the hippocampal neurons of rats with chronic mild unpredictable stress-induced depression / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of Shuyusan decoction on neuropeptide Y (NPY) and serotonin (5-HT) expression in the hippocampus and plasma of rats with chronic mild unpredictable stressors depression.</p><p><b>METHODS</b>Fifty Wistar rats were randomly divided into 5 groups, namely the normal control group, model group, fluoxetine group, and high- and low-dose Shuyusan groups. Except for those in the normal control group, all the rats were subjected to chronic mild unpredicted stress for 21 consecutive days with corresponding treatments. Open-field test was used to assess the behavioral changes of the rats. The content of NPY in the hippocampus and plasma was detected by competitive enzyme-linked immunosorbent assay, and immunocytochemistry was used to determine the expression of 5-HT in the hippocampus.</p><p><b>RESULTS</b>NPY levels in the hippocampus and plasma was significantly decreased in the model group as compared with that in the normal control group (P<0.05). Treatments with fluoxetine and high-dose Shuyusan both significantly increased NPY levels in the hippocampus and plasma in the depressive rats (P<0.05), resulting also in significantly increased 5-HT-immunoreactive neurons in the cerebral cortex and hippocampus and the average optical density (P<0.05).</p><p><b>CONCLUSION</b>Shuyusan decoction can effectively increase plasma and hippocampus NPY levels and the number of 5-HT-positive neurons in the cerebral cortex and happocampus of rats with chronic mild unpredictable stress-induced depression.</p>

Effects of baicalin against oxidative stress injury of SH-SY5Y cells by up-regulating SIRT1 / 药学学报

This study is to investigate the effect of baicalin (BL) against oxidative injury stress of SH-SY5Y cells induced by H2O2 and the possible mechanism. SH-SY5Y cells were pre-incubated with baicalin (25, 50, and 100 micromol x L(-1)) for 12 h prior to exposure to H2O2 (150 micromol x L(-1)) for 24 h. The viability of SH-SY5Y cells was measured by MTT assay. The contents of LDH and NO were determined. The percentage of apoptotic cells was assessed by flow cytometry (FCM). The content of Caspase-3 was tested by immunofluorescence histochemical method. BL at 50 and 100 micromol x L(-1) separately increased the cell viability and up-regulated SIRT1, reduced the contents of LDH, NO, Caspase-3 and the apoptotic percentage of SH-SY5Y cells. This study results suggest that baicalin could inhibit the H2O2-induced neuronal apoptosis. The further mechanism studies show that baicalin inhibit apoptosis via reducing Caspase-3 expression and up-regulating SIRT1.

Study on pancreas of type 1 diabetic mice induced by MLD-STZ using proteomics / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To get a better understanding of the mechanisms underlying type 1 diabetes mellitus, the differentially expressed pancreatic proteins from multiple low-dose streptozotocin (MLD-SIZ) mouse and normal mouse were analyzed and compared.</p><p><b>METHODS</b>20 male rats were separated into 2 groups (n=10): model mice treated with MLD-STZ and normal mice,differences of pancreatic proteome among in the two groups of mice, were analyzed by two dimensional polyacryamide gel electrophoresis (2DE). Protein quantification was analyzed and the differentially expressed spots were identified using mass spectrometry and MASCOT database searching.</p><p><b>RESULTS</b>Compared with control group, 23 proteins had changed significantly in the model group, 8 proteins expression were up-regulated, 15 proteins expressions down-regulated significantly. Using MALDI-TOF-MS, 15 proteins with significant change were identified by peptide fingerprinting map and the results were searched in MASCOT database. The function analyzed showed that proteins with change were associated with metabolic, anti-oxidant, structural, catalytic enzymes and chaperone, et al.</p><p><b>CONCLUSION</b>Type 1 diabetes is probably exerted via multi-target and multi-path mechanism. The proteins with significant change are newly target for type 1 diabetes early diagnosis and treatment.</p>

Expression of tau-related protein in spinal cord of patients with Alzheimer's disease / 中华病理学杂志

<p><b>OBJECTIVE</b>To study the expression of tau-related protein in spinal cord of Chinese patients with Alzheimer's disease.</p><p><b>METHODS</b>Gallays-Braak stain and immunohistochemical study for tau protein (AT8) were carried out in the spinal cord tissue (T2, T8, T10, L2 and S2 segments) of 3 Chinese patients with Alzheimer's disease. Seven age-matched cases without evidence of dementia or neurologic disease were used as controls.</p><p><b>RESULTS</b>Neurofibrillary tangles were identified in the neurons of anterior horn in 2 Alzheimer's disease cases but none was observed in the controls. Tau-positive axons and astroglia were detected in all Alzheimer's disease cases. Tau immunoreactivity in spinal cord of the patients correlated with that in brain tissue.</p><p><b>CONCLUSION</b>The expression of tau-related protein is demonstrated in the spinal cord of Alzheimer's disease patients suggesting that axonal transport defect may play a role in the pathogenesis of Alzheimer's disease.</p>

An experimental research of neuroglobin expression changes and neural apoptosis after traumatic brain injury / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To study the expression changes of neuroglobin in rats with the model of diffuse traumatic brain injury and explore the relationship between the neuroglobin and neuron apoptosis in traumatic brain injury.</p><p><b>METHODS</b>The diffuse traumatic brain injury of rats was induced by the Marmarou's 'weight-drop' device. And the immunohistochemical technique was used to detect the expression changes of neuroglobin and neuron apoptosis in rat brain at different time points post-injury.</p><p><b>RESULTS</b>The expression of neuroglobin increased twice and reached peaks at 2 hours and 72 hours post-injury respectively. And the increased expression of neuroglobin from 30 minutes to 1 hour post-injury and from 48 hours to 72 hours post-injury accompanied with the decreased expression ratio of Bax to Bcl-2.</p><p><b>CONCLUSION</b>The increased expression of neuroglobin in traumatic brain injury informed us that neuroglobin had anti-apoptosis action in post-injury neuron. It could protect the neuron from traumatic stress and secondary ischemia and hypoxia insults during ultra-early and acute stages.</p>

Pathologic diagnosis of non-Alzheimer type dementia / 中华病理学杂志

<p><b>OBJECTIVE</b>To characterize histopathologic features of non-Alzheimer type dementia.</p><p><b>METHODS</b>Bodian, Gallyas-Braak silver staining, tau and ubiquitin immunohistochemistry were applied in an analysis of 22 cases of autopsy-proven neurodegenerative dementia. Appearance, distribution and immunoreactivity of neuronal and glial inclusions in the brain were observed. The final histological diagnoses were made according to the pathological criteria for several types of common non-Alzheimer type dementia.</p><p><b>RESULTS</b>Among the 22 cases of neurodegenerative dementia, 12 cases were identified as non-Alzheimer type dementia, including Pick's disease (2 cases), progressive supranuclear palsy (3 cases) and corticobasal degeneration (3 cases), dementia with Lewy bodies (1 case), and Parkinson's disease (3 cases). Another 10 cases consisted of pure Alzheimer's disease (AD, 9 cases) and AD combined with argyrophilic grain disease (1 case). Characteristic neuronal and glial inclusions, such as classical and cortical Lewy body, Pick body, Globous NFTs, astrocytic plaque and tufted astrocyte, argyrophilic grain were found in the brains of non-Alzheimer type dementia. Classical and cortical Lewy bodies were not argyrophilic but were immunoreactive to ubiquitin. Pick bodies, Globous NFTs, astrocytic plaques, tufted astrocytes and argyrophilic grains were all argyrophilic. Pick bodies showed tau and ubiquitin immunoreactivity. However, Globous NFTs, astrocytic plaques, tufted astrocytes, and argyrophilic grains were reactive only to tau immunohistochemistry.</p><p><b>CONCLUSIONS</b>Findings of characteristic neuronal and glial inclusions may help to differentiate non-Alzheimer type dementia from AD, and in conjunction with Gallyas-Braak staining and immunohistochemistry for tau and ubiquitin, to further define histopathologic subcategories of non-Alzheimer type dementia.</p>

Morphological and quantatitive capillary changes in aging human brain / 中国医学科学院学报

<p><b>OBJECTIVE</b>To investigate morphological changes of capillary in aging brain and explore the role of vascular factor in brain aging.</p><p><b>METHODS</b>Twenty-eight brains of individuals (mean age 65 years) who died without clinical or pathological involvement of nervous system and 6 brains of Alzheimer's disease (AD) patients (mean age 83 years) were obtained at autopsy. Sections from frontal lobe, occipital lobe, striatum and hippocampus of normal subjects and sections from hippocampus of AD patients were used for hematoxylin eosin (HE), lox fast blue (LFB), toluidine blue stains and ulex europaeus agglutinin (UEA) immunostaining. After observations of morphological changes of neuron and capillary, computer-aid image analysis was performed to quantify numerical density and area density of neuron and capillary in frontal lobe, occipital lobe, putamen, CA3 sector of normal subjects and CA3 sector of AD patients. Numerical ratio and area ratio of neuron and capillary were then calculated. Correlations between neuron/capillary ratio and age were estimated using Pearson's correlation test. Difference of neuron/capillary ratio in CA3 sectors between AD patients and advanced aged normal subjects (> 75 years) was analyzed with Student's t-test.</p><p><b>RESULTS</b>Several pathological microvascular changes, including increased tortuosity, looping, bundling, stringing, and effacement of endothelia were seen in aged subjects and more prevalent in AD patients. Numerical ratio and area ratio of neuron and capillary of frontal lobe, occipital lobe and putamen significantly increased with age in normal aging subjects.</p><p><b>CONCLUSIONS</b>Morphological changes and relative decrease in number and capacity of capillary in aging brain may reduce cerebral blood flow and metabolism, and consequently result in functional impairment of aging brain. Vascular factors may play an important role in the development of brain aging.</p>