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Objective To study the expression of special AT-rich sequence-binding protein 1(SATB1) gene and its relationship with SLC22A18 protein expression in astrocytoma.Methods Fifty-six patients with astrocytomas (12 with grade Ⅰ,13 with grade Ⅱ,15 with grade Ⅲ,and 16 with grade Ⅳ),performed surgical excision in our hospitals from September 2006 to June 2010 and from September 2003 to June 2006,were chosen in our study; another 10 brain tissues from patients performed decompression operation resulting from cerebral hernia were selected as the controls.RT-PCR and Western blotting were used to detect the mRNA and protein expressions of SATB1.The SLC22A18 protein expression was detected by immunohistochemical assay.The relations between SLC22A18expressions and SA TB1 levels,and these two and the degree of malignancy were analyzed.Results RT-PCR and Western blotting revealed that positive mRNA and protein expressions were noted in 35patients with astrocytomas; the mRNA and protein expression rate and value of SATB1 in the astrocytoma tissues were significantly different among different grades of tumors (P＜0.05); the higher the malignancy grade,the higher mRNA and protein expression rate and value ofSA TB1; the protein expression value of SA TB1 had a positive correlation with the malignancy grade of tumors (r=0.987,P=0.000).And a few expressions of SA TB1 mRNA and protein were found in the tissues of controls.Immunohistochemical assay indicated that positive protein expression of SLC22A18 was noted in 19 astrocytoma tissues,and the protein expression rate of SLC22A18 in the astrocytoma tissues was significantly different among different grades of tumors (P＜0.05); the higher the malignancy grade,the lower expression of SLC22A18.And the protein expression of SLC22A18 was found in all the tissues of controls.The SATB1 expression rate in the tissues with negative SLC22A18 expression (81.1％) was significantly higher than that in the tissues with positive SLC22A18 expression (26.3％,P＜0.05).Conclusion SATB1 expresses in the astrocytoma tissues,indicating that it may play an important role in the pathogenesis of astrocytoma;up-regulation of SATB1 expression and dysfunction of SLC22A18 may play synergetic roles in the process of carcinogenesis of astrocytoma.
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Objective To investigate the morphological changes of different types of axonal injury in acute stage in rat brain with diffuse axonal injury(DAD caused by combined head injuries,and explore their relevant injury mechanisms. Methods SD rats were randomized into experimental (n=16)and normal control(=8)groups.According to the different injury times(6,24 h),the experimental group was equally divided into two subgroups(n=8).A new experimental facility was employed to induce DAI in rats.HE staining was conducted in different time points in the acute stage.Immunofluorescence assay was performed to detect the expressions of antibodies to β-Amyloid precursor protein(β-APP)and antibodies to neurofilament-68(NF-68)and electron microscope was also introduced to investigate the changes of axonemal ultrastructure.Results All injured rats experienced behavioral suppression:the coma in the experimental group was significantly prolonged as compared to that in the normal control group(P<0.05).Immunofluorescence assay for antibodies to β-APP and NF-68 revealed two distinct types of axonal injuly: β-APP confined to focal spheroidal axonal swellings and axonal retraction bulbs;while NF-68 Was only found within thin and elongate axonal segments. Electron microscope also demonstrated two different types of ultrastructure of axonal injury. Conclusion Impaired axonal transport and neurofilament compaction can occur independently in the process of axonal injury with different morphological changes.Multiple immunocytochemical approaches can help to fully assess the overall axonai response to traumatic brain injury.
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Objective To investigate the influence of nerve growth factor (NGF) on the level of plasma creatine kinase BB (CK-BB) and its clinical effect in patients with severe craniocerebral trauma. Methods Eighty patients with severe craniocerebral trauma (GCS≤8) were randomly assigned to NGF-treated (n=40) and control (n=40) groups. Conventional therapy was performed on these patients and NGF was added into the NGF-treated group. The level of plasma CK-BB in these patients was measured; the clinical prognosis of the patients was evaluated based on the GOS scores 6 months after severe craniocerebral trauma; the condition of regained consciousness was compared between the 2 groups. Results Plasma CK-BB in the NGF-treated group was significantly lower than that in the control group (P<0.05); the recovery rate in the NGF-treated group (24/40) was significantly higher than that in the control group (11/40); the consciousness regained within i month was found in 32 patients in the NGF-treated group but only 18 of that was noted in the control group (P<0.05); NGF-treated group (12.43±6.25) showed a significantly shorter time that consciousness was regained as compared with the control group (15.96±7.58). Conclusion NGF can decrease the level of plasma CK-BB, shorten coma time and improve life quality in patients with severe craniocerebral trauma. Application ofNGF, a safe and effective treatment method, provides a new potential therapeutic strategy for patients with CNS injury.
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Objective To investigate the effect ofstromal cell derived factor-1 (SDF-1) on the regulation of neural stem cells (NSCs) migration.Methods NSCs were obtained from the cerebral cortex of embryonic rats and cultured in serum-free medium,and their stem cell properties were assessed by means of induced differentiation in vitro into neurons and astrocytes.After in vitro cell culture,the purity of NSCs and the co-expression rate of CXCR4/nestin were detected by flow cytometry.Blind-well chambers were employed to detect the chemotactic effects of SDF-1 by counting the cells which had crossed a 8 μm pore membrane when confronted with varying concentrations of SDF-1 (0,1,10,50,100,500 and 1000 ng/mL),and the distribution of cells migrated out of the same neurosphere was overviewed by μ-slides in the persistent concentration gradient of SDF-1.Results Neurospheres were formed by persistent proliferation of NSCs, which were capable of differentiating into neurons (β-tubulin+) and astrocytes (GFAP+) in media without mitogens,and flow cytometry analyses showed that most of the cultured cells expressed nestin and the co-expression rate of CXCR4/nestin was nearly 80%.SDF-1 showed great chemotaxis to NSCs,and the amount of cells having migrated through the membrane in 500 ng/ml SDF-1 group was higher than that in other groups (P<0.05).When the cells were confronted with a linear concentration gradient (from 500 to 0 ng/mL),which was generated by diffusion and stable for at least 48 h,the cells migrated out ofa neruosphere could distribute irregularly with more cells locating in the region of higher concentration of SDF-1 and longer migration distance away from the center of the neurosphere than the opposite.Conclusion SDF-1 binding to its specific receptor CXCR4 was capable of inducing NSCs migrating directionally to the source of SDF-1.
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Objective To investigate the effect of recombinant human erythropoietin(rhEPO) on the activity of ATPase and superoxide dismutase(SOD) and malondialdehyde(MDA)content in the mitochondria of rat neurons after brain injury. Methods rhEPO was intraperitoneally injected in rats immediately after brain contusion injury induced by impact of a free-falling object.In the control rats,an equivalent volume of saline was injcoted intraperitoneally after the brain injury.At 6,12,24,and 48 hafter rhEPO or saline injection,the mitochondria were isolated from the brain neurons of the rats to determine the activity of ATPasc and SOD and the content of MDA.Results At 12.24 and48 h after rhEPO trealraent.the activity of ATPase and SOD increased and MDA content decreased significantly in the mitochondria of the brain neurons as compared with the measurements in the control group at the corresponding time points(P<0.05). Conclusion rhEPO treatment can ameliorate secondary brain injury in ratsfollowing brain trauma by modulating the mitochondrial function.
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Recently,the progress in employing transplanting stem cells to cure injured retina is very fast and has been continuously yielding exciting results.Various sources are used in the studies,including retina-derived cells such as M?ller cells and ciliary body cells,and non-retina-derived cells such as embryonic stem cells and brain-derived stem cells.This review briefly discusses the recent progress of these studies.
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<p><b>OBJECTIVE</b>To investigate the effects of magnesium sulfate on traumatic brain edema and explore its possible mechanism.</p><p><b>METHODS</b>Forty-eight Sprague-Dawley (SD) rats were randomly divided into three groups: Control, Trauma and Treatment groups. In Treatment group, magnesium sulfate was intraperitoneally administered immediately after the induction of brain trauma. At 24 h after trauma, total tissue water content and Na(+), K(+), Ca(2+), Mg(2+) contents were measured. Permeability of blood-brain barrier (BBB) was assessed quantitatively by Evans Blue (EB) dye technique. The pathological changes were also studied.</p><p><b>RESULTS</b>Water, Na(+), Ca(2+) and EB contents in Treatment group were significantly lower than those in Trauma group (P<0.05). Results of light microscopy and electron microscopy confirmed that magnesium sulfate can attenuate traumatic brain injury and relieve BBB injury.</p><p><b>CONCLUSIONS</b>Treatment with MgSO4 in the early stage can attenuate traumatic brain edema and prevent BBB injury.</p>