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ABSTRACT: To investigate the expression patterns of Msi1 and its relationship with tumour grading and angiogenesis in human glioma. Msi1 expression and the angiogenesis labelled by CD31 were detected by immunohistochemical staining in glioma from Grade I to Grade IV. MVD-CD31 was counted respectively in nuclear and cytoplasmic positive areas of Msi1. There was weak expression of Msi1 in the adjacent normal brain tissue of glioma, and there were less MVD-CD31 than in glioma. Glioma showed strong expression and different patterns of Msi1. From Grade I to Grade IV glioma, the expression pattern of Msi1 was changed from nuclear into cytoplasmic pattern gradually (P<0.05), and the expression patterns of Msi1 were related with the angiogenesis of glioma (P<0.05). It suggested that cytoplasmic Msi1 promoted angiogenesis and nuclear Msi-1 inhibited angiogenesis in glioma (P<0.05). Msi1 has different expression patterns in glioma from Grade I to Grade IV, and the different expression patterns play diverse roles in angiogenesis of glioma. This might explain that from Grade I to IV, glioma showed worse and worse prognosis.
Tissue and Cell 09/2012; · 1.04 Impact Factor
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ABSTRACT: The objective of this study was to explore the effects of Weichangshu tablets on free Ca²⁺ concentration of the gastrointestinal smooth muscle cells of rats and the molecular mechanism of the Weichangshu tablets. Cultured SD rat gastrointestinal smooth muscle cells were divided into control group, Cisapride group, Weichangshu group, and control + ethylene glycol tetraacetic acid (EGTA) group, Cisapride + EGTA group, and Weichangshu + EGTA group. Laser scanning microscope and spectrophotometer detection were applied to detect the calcium concentration. The calcium concentrations in Weichangshu group and Cisapride group significantly increased vs. control, and those in Weichangshu group were higher than those in Cisapride group. Ca²⁺ concentration in Weichangshu + EGTA group, Cisapride + EGTA group vs. control + EGTA group were not significantly different. Weichangshu could increase gastrointestinal smooth muscle free Ca²⁺ concentration, and this role may be achieved through the promotion of cells within the flow of calcium ions.
Journal of physiology and biochemistry 01/2011; 67(2):265-73. · 1.71 Impact Factor
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ABSTRACT: To explore the effect of nerve regeneration through repairing the defect of sciatic nerve in rats with the combination of optimized acellular allogeneic nerve and autologous neuroma.
30 SD rats were randomly divided into two groups A and B, with 15 in each, which were used in preparing the models of the autologous neuroma and the defect of sciatic nerve. In the group A, the combination of allogeneic nerve and autologous neuroma was transplanted; in the group B, the autogenous nerve was transplanted. 15 Wistar rats were used to provide acellular allogeneic nerve, which came from the sciatic nerve in one side of the leg. The electrophysiology examination, the evaluation of sciatic nerve function index and the histological examination were done at the 8th weeks and the 16th weeks after the operation.
At the 8th week, the limb escape response appeared in all rats; at the 16th week, there were many nerve fibers passing through the transplant in group A and group B. There was no significant difference in the number of the regenerated nerve fiber, diameter and the thickness of medullary sheath. At the 8th week, the conduction velocity of the regenerative nerve in group A were lower than that in group B (p < 0.05), and there was no statistical difference in two groups at the 16th week; there was no significant deviation in the function index of sciatic nerve in group A and group B(P > 0.05).
The combination of allogeneic nerve and autologous neuroma, which repairs the defect of peripheral nerve, can promote the regeneration of nerve, and the function of nerve conduction can be recovered, which is a good substitute of nerve grafts.
Turkish neurosurgery 10/2010; 20(4):470-9. · 0.62 Impact Factor
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ABSTRACT: Monosialoganglioside GM1 is a known neurotrophic factor. Nerve growth factor (NGF), a member of the neurotrophin family, is important for the survival, differentiation and maturation of neurons. The aim of this study was to test whether administration of GM1 and NGF can ameliorate glutamate (Glu) neurotoxicity in primary cultured embryonic rat dorsal root ganglia (DRG) and spinal cord neurons, and to investigate the mechanism underlying any effect. DRG and spinal cord neurons were exposed to the following treatments: Glu (2 mmol/L); Glu (2 mmol/L) plus GM1 (10mg/mL); Glu (2 mmol/l) plus NGF (10 ng/mL); Glu (2 mmol/L) plus GM1 (5mg/mL) and NGF (5 ng/mL). Cell viability was assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, ultrastructural alterations were examined using inverse phase contrast microscopy and electron microscopy, mitochondrial membrane potential was measured using rhodamine 123 labeling and flow cytometry, and neurofilament light (NF-L) mRNA expression was detected by reverse transcription-polymerase chain reaction. It was found that GM1 and NGF can increase the viability of neurons incubated with Glu, which, after GM1 and NGF treatment, were almost morphologically normal. The mitochondrial membrane potential of neurons was lowest for neurons treated with Glu alone, and that for neurons treated with Glu plus GM1 and NGF was higher than that for treatment with GM1 or NGF alone. The mRNA of NF-L was expressed at the highest level in neurons treated with Glu plus GM1 and NGF. Our findings indicate that NGF and GM1 act synergistically to protect DRG and spinal cord neurons from Glu cytotoxicity. NGF and GM1 may function by maintaining normal mitochondrial membrane potential or by promoting NF-L mRNA expression.
Journal of Clinical Neuroscience 02/2010; 17(4):495-500. · 1.25 Impact Factor
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ABSTRACT: Monosialoganglioside (GM1) has been considered to have a neurotrophic factor-like activity. Nerve growth factor (NGF), a member of the neurotrophin family, is essential for neuronal survival, differentiation and maturation. The aim of the present study was to investigate whether co-administration of GM1 and NGF reverses glutamate (Glu) neurotoxicity in primary cultured rat embryonic spinal cord neurons. Spinal cord neurons were exposed to Glu (2 mmol/l), Glu (2 mmol/l) plus GM1 (10 mg/ml), Glu (2 mmol/l) plus NGF (10 ng/ml), Glu (2 mmol/l) plus GM1 (5 mg/ml) and NGF (5 ng/ml) and then processed for detecting intracellular concentrations of Ca2+([Ca2+]i) by confocal laser scanning microscopy and growth associated protein 43 (GAP43) mRNA by RT-PCR. The fluorescent intensity in Glu plus GM1 and NGF incubated neurons was the lowest as compared with that in other groups. The expression of GAP43 mRNA in Glu plus GM1 and NGF incubated neurons was the highest as compared with that in other groups. These results implicated that GM1 and NGF have synergistic neuroprotective effects on spinal cord neurons with excitotoxicity induced by Glu in vitro.
Brain research bulletin 02/2009; 79(1):85-8. · 2.18 Impact Factor
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ABSTRACT: The aim of the present study was to determine whether the antidiabetic agent pioglitazone has a direct inhibiting effect on myocardial hypertrophy induced by high glucose and insulin in primary cultured neonatal rat cardiomyocytes. Culture preparations of ventricular muscle cells newborn rats were utilized. At 72 h of culture age, the cardiomyocytes were incubated for another 48 h with 25.5 mmol/L glucose plus 0.1 micromol/L insulin (group 2), 25.5 mmol/L glucose and 0.1 micromol/L insulin plus 10 micromol/L pioglitazone (group 3), 10 micromol norepinephrine (group 4), respectively. Cells cultured continuously in medium served as control (group 1). Cellular surface area, protein content, atrial natriuretic factor (ANF) mRNA, and cardiotrophin-1 (CT-1) mRNA were assessed after treatment with different agents. All those parameters increased significantly after treatment with high glucose and insulin as compared with control (P < 0.01). These effects were inhibited markedly by pioglitazone. The cellular surface area and ANF mRNA in group 3 were decreased as compared with group 2 (P < 0.01). The protein content and CT-1 mRNA in group 3 were also decreased as compared with group 2 (P < 0.05). We concluded that a the cellular level myocardial hypertrophy induced by high glucose and insulin was inhibited directly by pioglitazone in primary cultured cardiac myocytes. CT-1 may be involved in myocardial hypertrophy induced by high glucose andinsulin and inhibiting effects of pioglitazone on myocardial hypertrophy.
Pharmazie 01/2008; 62(12):925-9. · 1.01 Impact Factor
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ABSTRACT: To investigate whether butyrate increases substance P (SP) and calcitonin gene-related peptide (CGRP) release evoked by capsaicin from primary cultured dorsal root ganglion (DRG) neurons.
DRG was dissected out from embryonic 15-day-old Wistar rat and cultured as dissociate cells for 24 h then exposed to butyrate (0.01 mmol/L, 0.1 mmol/L, 1 mmol/L, 10 mmol/L, respectively) for another 48 h. The neurons cultured continuously in media served as normal control. All above cultured samples were processed for detecting expression of mRNA for SP, CGRP and vanilloid receptor 1 (VR1) of DRG neurons by RT-PCR, and VR1 protein expression by Western blot. SP and CGRP basal release levels were measured by radioimmunoassay (RIA). After that, the DRG cells for RIA were stimulated by capsaicin (300 nmol/L) for 5 min and the culture media were harvested for detecting SP and CGRP release levels by RIA. The neurons exposed to vehicle solution served as vehicle controls.
Exposure of butyrate on DRG neurons at higher concentrations (1 mmol/L, 10 mmol/L) for 48 h increased expression mRNA for SP and CGRP than that at lower concentrations (0.01 mmol/L, 0.1 mmol/L) and normal control (P<0.001). VR1 mRNA and VR1 protein expression increased in a dose-dependent manner after exposure of different concentrations of butyrate. Butyrate did not alter the basal release, significantly enhanced neuropeptide release evoked by capsaicin. SP and CGRP release levels in the culture media exposed by butyrate at higher concentrations (1 mmol/L, 10 mmol/L) for 48 h and then stimulated by capsaicin were higher than that at lower concentrations (0.01 mmol/L, 0.1 mmol/L) (P<0.001). The exposure of vehicle solution did not produce any increase of SP and CGRP release from primary cultured DRG neurons.
Butyrate may promote the expression of mRNA for SP, CGRP and increase sensitivity of capsaicin on SP and CGRP release from primary cultured rat dorsal root ganglion neurons. The promotion of VR1 mRNA and VR1 protein expression by butyrate implicated that VR1 may be involved in the mechanisms of sensory neuropeptide release evoked by capsaicin.
Neuro endocrinology letters 12/2006; 27(6):695-701. · 1.30 Impact Factor
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ABSTRACT: Monosialoganglioside (GM1) has been considered to have a neurotrophic factor-like activity. Nerve growth factor (NGF), a member of the neurotrophin family, is essential for neuronal survival, differentiation and maturation. The aim of the present study was to investigate whether co-administration of GM1 and NGF reverses glutamate (Glu) neurotoxicity in primary cultured rat embryonic dorsal root ganglion (DRG) neurons. DRG neurons were exposed to Glu (2 mmol/1), Glu (2 mmol/1) plus GM1 (10 microg/ml), Glu (2 mmol/l) plus NGF (10 ng/ml), Glu (2 mmol/l) plus GM1 (5 microg/ml) and NGF (5 ng/ml) and then processed for detecting intracellular concentrations of Ca2+ ([Ca2+] i) by confocal laser scanning microscopy and growth-associated protein 43 (GAP43) mRNA by RT-PCR. The fluorescent intensity in Glu plus GM1 and NGF incubated neurons was the lowest as compared with that in other groups. The expression of GAP43 mRNA in Glu plus GM1 and NGF incubated neurons was the highest as compared with that in other groups. These results implicated that GM1 and NGF have synergistic neuroprotective effects on DRG neurons with excitotoxicity induced by Glu in vitro.
Nutritional Neuroscience 10(3-4):105-11. · 1.56 Impact Factor
