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Objective To investigate the changes of brain edma and expression of blood high mobil-ity group box 1(HMGB1) and calcium binding protein S100B after traumatic brain injury (TBI) in IL-4 knockout (IL-4 KO) mice,and to explore the effects of IL-4 on traumatic brain injury. Methods Twenty male wild type ( WT) or twenty male IL-4 KO BALB/cJ mice were randomly divided into WT sham TBI group,WT TBI group,IL-4 KO sham TBI group and IL-4 KO TBI group(n=10 in each group).The model of traumatic brain injury was established by the free falling body epidural impact method,then the brain water content was measured. The expression of aquaporin-4 ( APQ4) and HMGB1 in injured brain of each group was detected by Western blot,and the concentration of HMGB1 and S100B in serum was detected by ELISA assay. Results ( 1 ) The brain water content of injured lateral brain of BALB/cJ mice with IL-4 gene knockout was significantly higher than that of wild type mice with brain injury model (WT group: (80.03± 0.35)％;IL-4 KO group:(81.93±0.41)％;P<0.05).(2) The Western blot showed that the expression of AQP4 and HMGB1 in brain tissue of BALB/cJ mice with IL-4 gene knockout was significantly higher than those in wild type mice after traumatic brain injury. ( 3) The results of ELISA showed that the levels of HMGB1 and S100B in the serum of IL-4 knockout BALB/cJ mice were significantly higher than those of wild type mice (HMGB1:WT group:(9.21±0.74)ng/ml;IL-4 gene knock-out group:(13.39±1.33)ng/ml,P<0.05;S100B protein:WT group:(11.11±0.84)pg/ml;IL-4 KO group: (18.11±2.02)pg/ml,P<0.05 ). Conclusion The brain tissue water content and the expression of APQ4 are increased in IL-4 KO TBI mice.The expression of HMGB1 in brain issue and serum and S100B in serum are also up-regulated.
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@# Diabetes mellitus can cause central nervous system dysfunction. Astrocyte, as an important part of the central nervous system,is affected by diabetes, which involve the volume of astrocyte, intercellular gap junctions, the expression of protein, glycogen storage and so on.
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ObjectiveTo explore the effects of fluoxetine on special learning and memory and serum S100B level in depressed model rats.MethodsAdult male SD rats were divided into six groups randomly according random digits table:control group ( A ),depressed model group ( B ),group of depressed model treated with single dose of fluoxetine for one day ( C ),group of depressed model treated with fluoxetine for one week (D),group of depressed model treated with fluoxetine for two weeks (E) and group of depressed model treated with fluoxetine for four weeks (F),ten rats in each group.Except control group,others were subjected to forced-swimming for four weeks,15 min a day.Fluoxetine (10 mg/kg) was given intragastric administration to group C-F before swimming everyday.Morris water maze ( MWM ) was used to measure the spatial learning and memory of rats.ELISA was used to determine the level of serum S100B.ResultsIn the hiding platform test of MWM,there was significant longer of escape latency (EL) in B group than that in A group(P ＜ 0.05 ).And the EL in all groups treated with fluoxetine became shorter with the prolonging of treatment.In the probe test,there were significant longer time in target quadrant in D,E,F than in other quadrant (F =5.162,P ＜ 0.01 ).The levels of serum S100B were lower in E,F groups ( E group ( 0.91 ± 0.23 ) ng/ml,F group ( 0.85 ± 0.21 ) ng/ml) than that in B group (( 1.26 ±0.61 )ng/ml,P＜0.05).ConclusionChronic administration of fluoxetine could improve the impairment of spatial learning and memory and reverse the increase of S100B level in serum of depressed model rats.
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Objective To evaluate the metabolite pattern and the severity in patients with spinocerebellar ataxia type 3/ Machado-Joseph disease (SCA3/MJD) by 1H magnetic resonance spectroscopy (1H-MRS) on different cerebellar regions, including cerebellar vermis, cerebellar peduncles, cerebellar cortex, and dentatum. Methods Thirty-six SCA3/MJD patients, and 27 sex, age-matched healthy controls were scanned with 1H-MRS for N-acetylaspartate (NAA), choline (Cho) and creatine (Cr). We made cerebellar vermis, cerebellar peduncles, cerebellar cortex, and dentatum as the region of interests (ROI), and finally got access to NAA/Cr, Cho/Cr, and NAA/Cho ratios. We also examined the CAG repeat numbers of MJD1 gene, scored the 36 patients by the scale for the assessment and rating of ataxia (SARA), analyzed the differences in ratios between SCA3/MJD patients and the control group, and explored whether relevance existed between these ratios and duration of the disease, age of onset, CAG repeat times, and SARA scores respectively. Results The ratio of NAA/Cr in SCA3/MJD patients showed a significant reduction in the cerebellar cortex, dentatum, cerebellar vermis and medipeduncle (P<0.01) compared with the controls. The ratio of NAA/Cho also showed significant reduction in the dentatum and cerebellar vermis (P<0.01). A number of correlations were found between the metabolite ratios of 1H-MRS and duration of the disease, age of onset, expanded CAG and SARA score in SCA3/MJD patients. Conclusion 1H-MRS, which shows the neural metabolic changes in the cerebella of SCA3/MJD patients, provides useful information about the severity of SCA3/MJD.
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Objective To determine the neuronal damage or loss and gliosis at the cellular level in spinocerebellar ataxia type 3/Machado-Joseph disease(SCA3/MJD), and evaluate the potential use of neuron-specific enolase (NSE) and protein S 100 B(S100B) serum concentrations as biochemical markers. Methods Serum concentrations of NSE and S100B were measured in 102 SCA3/MJD patients and 100 healthy subjects matched by sex and age. The correlations between both markers and age, age of onset, disease duration, CAG repeat size, scores of international cooperative ataxia rating scale(ICARS), and scale for the assessment and rating of ataxia(SARA) were analyzed. Results Compared with the healthy controls, patients with SCA3/MJD had higher NSE serum concentrations [(6.95±2.83)ng/mL vs (4.83±1.70) ng/mL, P<0.05] and higher S100B serum concentrations [(0.07±0.06) ng/mL vs (0.05±0.02) ng/mL, P<0.05]. In the SCA3/MJD patients group, NSE levels presented a positive correlation with age, disease duration, ICARS scores and SARA scores, whereas S100B levels did not correlate with age, age of onset, disease duration, ICARS scores and SARA scores. CAG repeat size did not correlate with the NSE levels and S100B levels in different age groups of SCA3/MJD patients. Conclusion Serum NSE might be a useful marker to monitor disease progression and represent the degree of severity of a certain disease. Elevated S100B serum concentrations in patients compared to healthy controls may suggest an application of this protein as a peripheral marker of brain impairment in SCA3/MJD.
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A proteína S100B cerebral tem sido utilizada como um marcador periférico de injúrias do sistema nervoso central (SNC). Entretanto, estudos recentes demonstraram que a S100B também aumenta após o exercício físico, embora o significado desse aumento ainda não esteja bem claro. Apesar de ser liberada, principalmente, por astrócitos, no sistema nervoso central, fontes de produção extracerebral de S100B durante o exercício podem estar implicadas no aumento sérico desta proteína. No entanto, exercícios que implicam impacto ao cérebro como o boxe, por exemplo, o aumento é claramente associado à lesão cerebral. Assim, trabalhos propõem que o aumento da S100B após o exercício estaria relacionado à secreção ativa por adipócitos e músculos lesados. Uma vez que a liberação da S100B pelo músculo lesado seja confirmada experimentalmente, o uso desta proteína poderia ser aprofundado,principalmente, no treinamento esportivo. Atualmente, estamos desenvolvendo protocolos na direção de avaliar o potencial valor da S100B como indicador de lesão do músculo esquelético. Portanto, o objetivo da presente revisão é apresentar o atual estado de conhecimento sobre a relação entre a proteína S100B e o exercício físico, discutindo os possíveis mecanismos envolvidos e propondo novas abordagens.
Protein S100B has been used as a peripheral biochemical marker of brain injury and/or activity. However, recent studies have demonstrated that this protein is also increased in serum after physical exercise, although the interpretation of this finding remains controversial. Although predominantly released by astrocytes in the central nervous system, extracerebral sources of protein S100B have been suggested to contribute to the increase in serum levels of this protein. However, in the case of exercises that have an impact on the brain such as boxing, elevated levels are clearly associated with brain damage. More recently, some studies have proposedthat protein S100B might be released by activated adipocytes and by damaged muscle cells. If confirmed experimentally, protein S100B might be potentially useful in sports training. We are currently investigating the potential role of serum protein S100B as an indicator of muscle damage. Therefore, the objective of this review was to discuss the current knowledge about the relationship between physical exercise and serum protein S100B and its possible leakage from muscle cells injured by exercise.
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Objective To observe the influence of δ-opioid reperfusion in rats with change in serum protein S-100B level and to explore the neuroprotective effect of DADLE during cerebral resuscitation. Method The model of global cerebral ischemia and reperfusion was induced by bilateral common carol id artery occlusion combined with hypotension. Fifty SD rats were randomly divided into five groups: sham operation group, model group, DADLE pretreated group, DADI.E treated postischemia group, DADLE treatment during reperfusion group ( n = 10 for each group) .In sham operation group,the rats were operated without ischemia and treatment; in model group, rats had global cerebral ischemia and reperfusion model up without any treament; in DADLE pretreated group, rats received DADlE before ischemia; in DADLE treatment postischemia group,rats had DADLE immediately after ischemia; in DADLE treatment during reperfusion group,rats got DADLE during early reperfusion. After the establishment of model, serum protein S-JOOB was measured by using ELlSA.One-way analysis of variance and SNK test were used for comparison between groups. Results The serum protein S-100B level was (475.56±1.93) pg/ml in sham operational group and that was much lower than that in model group and DADLE treatment groups. While the levels of serum protein S-100B in all DADLE treatment groups were reduced significantly in comparison with model group. There were no differences in the levels of serum protein KS-100B between DADLE treatment groups. Conclusions The δ-opioid receptor DADLE exerts neuroprotective effects on global cerebral ischemia and reperfusion in rats.
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Objective To investigate the relationship between serum protein S100b in intracerebral hemorrhage (ICH) patients and brain damage. Methods A total of 37 hypertensive cerebral hemorrhage patients, 24 male and 13 female, were enrolled as intracerebral hemorrhage (ICH) group, aged from 45 to 85 years with an average of (69.2?8.9) years. The control group were matched with ICH group, including 30 healthy subjects, 19 male and 11 female, aged 52 to 70 (61.2?5.0) years. The concentration of serum protein S100 was detected using double antibody sandwich ELISA. Evaluation of blood volume was calculated with the fomula based on cranial CT data: V=S?L?Slice??/6. The nerve function of the patients was evaluated by the CSS during acute phase and Barthel index score at 3 month after stroke. Results Serum protein S100 concentration was significantly elevated in patients with ICH (0.54?0.41 ?g/L), as compared to controls (0.17?0.04 ?g/L)(P