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OBJECTIVE@#To explore the expression profile of Ephrin-B2 in the ischemic penumbra after transient focal cerebral ischemia in rats, and to clarify the mechanism of Ephrin-B2 triggering angiogenesis.@*METHODS@#Sprague-Dawley rats were randomly divided into a normal group, a sham operation group and ischemic-reperfusion 1, 3, 7, 14, and 28 d groups. Suture-occluded method was used to establish the focal middle cerebral artery occlusion model and the ischemic brain was reperfused 2 h after the occlusion. Western blot and quantitative real-time reverse-transcription polymerase chain reaction were used to detect the dynamic expression profile of Ephrin-B2 in the penumbra cortex. Double immunofluorescence was used to speculate the location and the co-expression of Ephrin-B2 in blood vessels, neurons and astrocytes. Microvessel density was quantified by the number of CD31+ cells. Rats were subjected to neurologic functional tests by modified neurological severity scores (mNSS) before sacrifice.@*RESULTS@#Compared with the sham group, Ephrin-B2 protein and mRNA level of the penumbra cortex in the ischemic group increased 3 days (P<0.05) after the reperfusion, peaked at day 7 and 14 (P<0.01), and declined at day 28. Double immunofluorescence indicated that Ehprin-b2 was expressed in the neurons, blood vessels and astrocytes; mNSS peaked at day 7, and gradually declined at day 14. The microvessel density of penumbra cortex in the ischemic group increased 3 days (P<0.05) after the reperfusion, peaked at day 14 (P<0.01), and gradually declined at 48 h.@*CONCLUSION@#Cerebral ischemia reperfusion induces the over-expression of Ephrin-B2, with a dynamic trend, suggesting that Ehprin-b2 may improve post-stroke functional recovery by enhancing angiogenesis and neurogenesis.
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Animaux , Rats , Astrocytes , Métabolisme , Encéphale , Anatomopathologie , Encéphalopathie ischémique , Métabolisme , Cortex cérébral , Métabolisme , Éphrine B2 , Métabolisme , Infarctus du territoire de l'artère cérébrale moyenne , Accident ischémique transitoire , Neurones , Métabolisme , Rat Sprague-Dawley , Lésion d'ischémie-reperfusion , MétabolismeRésumé
OBJECTIVE@#To explore the association between apolipoprotein AI (ApoAI) gene rs12721026 polymorphism and cerebral hemorrhage (CH) in Changsha Han population, and to evaluate the effect of rs12721026 polymorphism on plasma lipid levels.@*METHODS@#A total of 273 patients with CH and 140 healthy controls were collected. The rs12721026 polymorphism of ApoAI was analyzed by SNaPshot genotyping analysis and DNA sequencing. The total cholesterol (TG), triglyceride (TC), HDL-C and LDL-C were examined by oxidase method.@*RESULTS@#There was no significant difference in the genotype and allele frequencies of rs12721026 polymorphism between the CH group and the control group (P>0.05). Both in the CH group and in the control group, the level of HDL-C of the TT gene type of rs12721026 was significantly higher than that of the GT/GG gene type (P<0.05). There was no significant difference in the levels of TG, TC and LDL-C among different subgroups of gene types.@*CONCLUSION@#There may be no association between apoAI gene rs12721026 polymorphism with CH in Changsha Han population, which may still influence the HDL-C levels.
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Humains , Apolipoprotéine A-I , Génétique , Asiatiques , Études cas-témoins , Hémorragie cérébrale , Sang , Génétique , Cholestérol , Sang , Fréquence d'allèle , Génotype , Lipides , Polymorphisme de nucléotide simple , Analyse de séquence d'ADN , Triglycéride , SangRésumé
Objective To observe the effect of tetrahydroxy stilbene glucoside (TSG) on the behavior on rat model and the expressions of autophagy-associated protein Beclin-1 and LC3- Ⅱ induced by Aβ1-42 Methods Eighty rats were equally randomized into 4 groups (n =20):The control group,the sham operated group,the model group and the TSG group.The behavior of rats was measured by using Y-maze and Morris water maze.The expression of Beclin-1 and LC3- Ⅱ in rats hippocampus was detected by Western blot and RT-PCR at the time points.Results The number of electric-stimulus in hippocampus significantly increased and the Morris water maze test showed that the escape latency prolonged,swimming distance increased and the times of crossing the exact former platform location decreased both in the model and TSG groups after 21 days compared with those in control group.The mRNAs and protein expressions of Beclin-1 (0.51 ±0.03)and LC3-Ⅱ (0.68 ± 0.04) in model group were higher than that in control group (0.31 ± 0.01,0.31 ± 0.02) at that time point ( Beclin-1:t =28.2843,P < 0.05 ; LC3- Ⅱ :t =37.0000,P <0.05).Compared to model group,the expression of the Beclin-1 and LC3- Ⅱ was decreased at 21 d in TSG group (Beclin-1:t =9.8387,P < 0.05 ; LC3- Ⅱ :t =16.2698,P < 0.05 ).Conclusions Autophagy self-regulated system is started through the increased expressions of Beclin-1 and LC3- Ⅱ after Aβ deposition in rats,so as to attenuate cerebral injury caused by Aβ neurotoxicity.Autophagy pathway is possible one of the mechanisms in Aβ neurotoxic injury. Tetrahydroxy stilbene glucoside from polygonum multiflorum has protective effect on it.
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Objective To explore the expression of vascular endothelial growth factor (VEGF)mRNA and protein in endothelia progenitor cells (EPCs) and VEGF in the culture medium and serum of patients during acute period of cerebral hemorrhage associated with hypertension (APCHH). Methods Mononuclear cells from peripheral blood of patients with APCHH ( 16 patients) and hypertension ( 16 patients) were isolated and induced to EPCs. Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis was performed to assay VEGF mRNA. VEGF protein was assessed by Western blotting. The VEGF protein level in patient's serum and culture medium ( at day 7 ) were assayed using VEGF ELISA Kit and compared between APCHH group and hypertension group. Results Compared with hypertension group, VEGF mRNA (0. 186 ±0. 035 versus 0.090 ±0.031, t =8.318, P <0.0l ) and protein (0. 223 ± 0. 028 versus 0.169 ± 0. 022, t = 3. 744, P < 0. 01 ) expression of EPCs, the concentration of VEGF protein in the supernatant (414 ±37 versus 316 ±29, t =8. 270, P <0. 01 ) and in serum (408 ±49versus 222 ±34, t = 12.406, P <0. 01 ) were all significantly increased in APCHH group. Conclusion The VEGF protein levels in serum of patients and in the culture medium, VEGF mRNA and protein expression in EPCs were all significantly increased during acute periods of cerebral hemorrhage.
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Objective To explore the relationship between lecithin cholesterol acy ltransferase (LCAT) gene 608C/T and 511C/T polymorphisms and stroke in Chinese Han population in Hunan province. Methods One hundred fifty patients with cerebral infarction, 150patients with cerebral hemorrhage, and 122 age- and sex-matched healthy controls were selected.LCAT gene 608C/T and 511C/T polymorphisms were detected by using polyrnerase chain reaction, single strand conformation polymorphism, and restriction fragment length polymorphisms. Results The CT genotype frequency (14. 0% ) and T allele frequency (7. 0% )of the LCAT gene 608C/T in the cerebral infarction group were significantly higher than those in the control group (all P <0. 05), while there were no significant differences in the CT genotype frequency (7. 3% ) and T allele frequency (3.7%) between the cerebral hemorrhage group and the control group (P > 0. 05). The CT genotype frequency (10. 0% ) and T allele frequency (5. 0% ) of the LCAT gene 511C/T in the cerebral infarction group were significantly higher than those in the control group (all P <0. 01), while there were no significant differences in the CT genotype frequency (3.3%) and T allele frequency (1.7%) between the cerebral hemorrhage group and the control group (P >0. 05). Conclusions The 608C/T and 511C/T polymorphisms may be associated with the occurrence of atherosclerotic cerebral infarction in Chinese Han population in Hunan province. They may be the predisposing factors for atherosclerotic cerebral infarction in this population; however, they are not associated with cerebral hemorrhage.
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OBJECTIVE@#To investigate the relation between C923T(Ala308Val)polymorphism in exon 10 of neutrophil cytosolic factor 1 (NCF1) gene and cerebral hemorrhage in the Han in Changsha and to evaluate the effect of C923T(Ala308Val) polymorphism on plasma lipid levels.@*METHODS@#Changsha Han C923T(Ala308Val)polymorphism in NCF1 gene was determined by PCR single strand conformation polymorphism analysis and DNA sequencing in 100 healthy controls, 110 patients with cerebral hemorrhage, and 10 cerebral hemorrhage pedigrees. The level of plasma lipid was measured by routine methods.@*RESULTS@#No significant difference was found in frequencies of genotypes and alleles of C923T(Ala308Val)polymorphism among the controls, cerebral hemorrhage patients and cerebral hemorrhage pedigrees. The serum level of TG in the CT genotype of cerebral hemorrhage patients and controls tended toward higher than that in CC genotype, but the trend did not reach significance (P>0.05).@*CONCLUSION@#There seems no correlation between C923T(Ala308Val)polymorphism and cerebral hemorrhage in Hans people in Hunan province.
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Femelle , Humains , Mâle , Asiatiques , Génétique , Séquence nucléotidique , Hémorragie cérébrale , Génétique , Chine , Données de séquences moléculaires , NADPH oxidase , Génétique , Polymorphisme génétique , Espèces réactives de l'oxygène , MétabolismeRésumé
@#ObjectiveTo study the protective effects of 2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glucoside(TSG) on the PC12 cells injury induced by H2O2.MethodsAll cells were divided into 5 groups: the saline control group(control group), Oxidative damage PC12 cells model group(H2O2 group) which was induced by H2O2, and TSG treated group, which oxidative damage PC12 cells model which was induced by H2O2 after given TSG 2 h at TSG 120 μg/L(TSG 120 μg/L+H2O2 group), 60 μg/L(TSG 60 μg/L+H2O2 group) and 30 μg/L(TSG 30 μg/L+H2O2 group) once. The survival rate of the cells was determined by MTT method, the content of lactate dehydrogenase (LDH) was determined by ultraviolet spectrophometry and the content of malonyldialdehyde (MDA) and superoxide dismutase (SOD) activity was measured respectively by thiobarbituric aicd and xanthine oxidese method. Immunohistochemitry method were used to detect the expression of bcl-2.ResultsTSG reduced obviously cells injury induced by H2O2. 30~120 μg/L TSG improved the cells survival rate, reduced LDH releasing and MDA content, increased SOD activity, and decreased the expression of bcl-2 in the PC12 cells injury induced by H2O2(P<0-05, P<0-01). ConclusionTSG has significantly potective effect on the PC12 cells injury induced by H2O2.
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Objective To observe the effect of supernatant liquid from brain tissue on the differentiation of adipose-derived stem cells (ADSCs) into neural cells in normal brain tissues, the homogenate of infarcted cerebral hemisphere and the opposite side in the rats. Methods The ADSCs were obtained from rat retroperitoneal adipose tissue. The normal brain tissues, the homogenate of the infarcted cerebral hemisphere and thc opposite side got from middle cerebral artery occlusion in rats were used to induce ADSCs. Immunocytochemistry or immunofluorescence were used to identify the cell types at the 3rd day. Positive expression rate was counted by fluorescence microscope. Results (1)The neuron-specific enolase (NSE) positive cells, microtubule-associated protein 2 (MAP-2) positive cells and glial fibrillary acidic protein (GFAP) positive cells were much more in the homogenate of the infracted cerebral hemisphere than in others (P<0.05). (2)The NSE positive cells, MAP-2 positive cells and GFAP positive cells were much more in the homogenate of the normal brain tissues and the opposite side than normal level ( P < 0. 05 ) . Conclusions The homogenate of the infracted cerebral hemisphere and the opposite side can induce adipose-derived stem cells into neural-like cells and express neural cells markers in rats.
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Objective To investigate the relationship between C1773T polymorphism of LDL receptor gene (LDLR) and cerebral hemorrhage and the impact of C1773T polymorphism of LDLR on the levels of serum lipids in Chinese Han in Changsha, Hunan province. Methods Two hundred seventy-three cerebral hemorrhage patients and 140 normal controls were recruited in the present study. The C1773T polymorphism of LDLR was analyzed by SNaPshot and direct DNA sequencing. The triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C) and low density lipoprotein-cholesterol (LDL-C) levels were examined using oxidase method. Results The CC, CT and TT genotype frequencies of LDLR polymorphism were 0.703/0.278/0.019、0.707/0.250/0.043 and the allele C and T frequencies of LDLR polymorphism in the cerebral hemorrhage group and the control group were 0.842/0.158,0.832/0.168 respectively. The differences in genotype and allele frequencies of LDLR polymorphism were no significant between cerebral hemorrhage group and the control group (P>0.05). There were no significant differences in the levels of lipids among the CC, CT and TT genotype in either cerebral hemorrhage group or the control group (P>0.05). Conclusions The LDLR-C1773T polymorphism may not be associated with cerebral hemorrhage nor be related to hyperlipemia in Chinese Han in Changsha.
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OBJECTIVE@#To explore the association between single nucleotide polymorphism (SNPs) of KLK1 gene and cerebral hemorrhage in Changsha Han population.@*METHODS@#We enrolled 273 patients with cerebral hemorrhage and 140 normal people. The SNPs (including rs3212855 and rs5515) of KLK1 gene were analyzed by Snapshot method and direct sequencing.@*RESULTS@#We found rs5515 was not a polymorphic site in Changsha Han population. Genotype and allele frequency in rs3212855 were not different between patients with cerebral hemorrhage and the controls (P>0.05). The blood pressure level was not different between the genotype subgroups.@*CONCLUSION@#Neither rs5515 nor rs3212855 is associated with cerebral hemorrhage.
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Adolescent , Adulte , Sujet âgé , Sujet âgé de 80 ans ou plus , Femelle , Humains , Mâle , Adulte d'âge moyen , Jeune adulte , Hémorragie cérébrale , Génétique , Chine , Ethnologie , Génotype , Kallicréines , Génétique , Polymorphisme de nucléotide simple , GénétiqueRésumé
OBJECTIVE@#To investigate the neuroprotective mechanism of tetrahydroxystilbene glucoside (TSG), a Chinese medicine, on rats after cerebral ischemia-reperfusion.@*METHODS@#A total of 96 Sprague-Dawley male rats were divided into 4 groups (n=24): a control group, an ischemia-reperfusion (I/R) model group, a low dose TSG [60 mg/(kg.d)]group, and a high dose TSG [120 mg/(kg.d)]group. After 6 days intragastric (ig) administration of TSG or natural saline (I/R group), reversible middle cerebral artery occlusion (MCAO) model was established by intraluminal suture technique. The rats of control group were operated on while the middle cerebral artery was not blocked. At 6 h, 24 h, 48 h, and 7 d after the reperfusion, behavior test was used to evaluate the neurological deficiency of each group. The protein expressions of nerve growth factor (NGF), growth associated protein (GAP)-43, and protein kinase A catalytic subunit (PKAc) in the cortex were measured by immunohistochemical method.@*RESULTS@#Compared with the I/R group, the neurological defect scores of the 2 TSG groups were significantly lower except at 6 h after the reperfusion. Compared with the I/R group, the protein expression of NGF, GAP-43, and PKAc after the reperfusion of the 2 TSG groups increased significantly.@*CONCLUSION@#The protein expression of NGF may increase when treated with TSG after cerebral ischemia-reperfusion, which activates the PKA pathway and increases the protein expression of GAP-43 that protects the neuron.
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Animaux , Mâle , Rats , Protéine GAP-43 , Métabolisme , Glucosides , Pharmacologie , Utilisations thérapeutiques , Infarctus du territoire de l'artère cérébrale moyenne , Traitement médicamenteux , Facteur de croissance nerveuse , Métabolisme , Neuroprotecteurs , Pharmacologie , Utilisations thérapeutiques , Répartition aléatoire , Rat Sprague-Dawley , Lésion d'ischémie-reperfusion , Stilbènes , Pharmacologie , Utilisations thérapeutiquesRésumé
BACKGROUND: Basic fibroblast growth factor (bFGF) can accelerate the bone marrow mesenchymai stem cells (BMSCs) proliferation and differentiation into nerve cells, which is considered as a mitogen of glial cells.OBJECTIVE: To investigate the survival and differentiation of bFGF gene modified BMSCs transplanted on rat models of cerebral ischemia by double immunofluorescence staining, and to study the differentiation trend of BMSCs into neuron-like cells and glial cells.DESIGN, TIME AND SETTING: The randomized control animal experiment was completed in the central laboratory of Experimental Animal Center of Central South University from July 2005 to March 2006.MATERIAL: Fifty Sprague-Dawley rats were divided into 4 groups at random: sham operation group (n=10), cerebral ischemia-reperfusion injury group (n=10), BMSCs group (n=i5) and bFGF modified BMSCs group (n=15). METHODS: Except sham operation group, rats in the other three groups were prepared for local cerebral ischemia-reperfusion models. Then BMSCs or bFGF modified BMSCs were intravenously transplanted into cerebral ischemic rats, and the same volume of DMEM were injected in the cerebral ischemia-reperfusion injury group. MAIN OUTCOME MEASURES: Survival rate and differentiation of grafted cells were observed by 5-bromo-2-deoxyuridine (BrdU)-NeuN, and BrdU-glial fibrillary acidic protein (GFAP) double immunofluorescence staining; the neurological scores and infarction volumes in each group. RESULTS: At 7 days after implantation, the number of BrdU/NeuN-positive cells and BrdU-GFAP-positive cells in the bFGF modified BMSCs group was higher than those on the BMSCs group (P < 0.05), but there were no significant differences in the co-expression cells by double immunofluorescence staining between the two groups (P > 0.05). At 7 days following reperfusion, neural function of cerebral ischemia rats were improved and infarction volume was reduced in both BMSCs group and the bFGF modified BMSCs group, and bFGF modified BMSCs group was superior to BMSCs group. CONCLUSION: BMSCs modified by bFGF can survive in cerebral ischemic region and differentiate into neuron and glial cells, which are more proper for repairing nerves.
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@#Regeneration of axon was play an important role in the functional repair after spinal cord injury,and it was affected by vascular damage,absent availability nutrition transportation,urged to be solved.Inducing angiogenesis by electrical fields might be benefit to enhance anatomical plasticity and recovery of function after spinal cord injury.
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Objective To study that Geranylgeranylacetone(GA) induce the expression of heat shock protein 70 expression in hippocampus of Alzheimer's model rats and its effect on learning and memory ability in the model rats induced by Aβ1-42 injection into hippocampus.Method 72 health SD rats were randomly divided into GGA group,model group was injected with Aβ1-42 and control group was injected with normal saline into hippocampus.Y maze test was used to detect the learning and memory ability of the rats at the 7th,14th and 21st day after injection into hippocampus separately.HSP70 expression in hippocampus tissues were detected by RT-PCR and western-blot as soon as Y maze test has been finished.Result The learning and memory ability of the rats in model group decreased significantly at the 14th and 21st day after injection than those in control group(P<0.05),but not too much changed in GGA group(P<0.05).HSP70 expres- sions in hippocampus tissues in model group decreased gradually after injection Aβ1-42,but increased in GGA group at the 7th,14th and 21st day after injection.Conclusion GGA can induce the expression of HSP70 in hippocarnpus of Alzheimer's model rats and meliorate the neuron impairment as well as the learning and memory ability of the rats.
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Objective To investigate the association of the tumor necrosis factor ligand superfamily member(TNFSF)4 gene polymorphisms rs3861950 and cerebral infaretion in Hunan area.Methods The frequencies of the genotypes of rs3861950 were detected utilizing real-time fluorescent PCR method based on TaqMan probe.Subiects examined were composed of 287 patients and 285 healthy individuals.Results There were significant differences in TNFSF4 gene rs3861950 C→T site polymorphism and allele frequency between the subjects and the controls,the distribution of CC genotype was significantly higher in the former (7.7%)than in the later(2.1%,X2=9.553,P=0.008),so was the frequencies of C allele(0.190 vs 0.137,X2=5.887,P=0.015).Moreover,there were significant differences in the distribution of genotype and the frequencies of allele between the subgroup of cerebral thrombosis and control group ( for the distribution of genotype X2=9.396 P=0.009,for the frequencies of allele X2=6.134,P=0.013).Logistic regression analysis showed that the risk factor of CC genotype was 3.7 times higherthan others(P=0.002.OR 3.706).Conclusions TNFSF4 gene SNP rs3861950 is associated with cerebral infarction and C allele is considered to be one of independent risk factors in the Han population in Hunan Province.
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Objective To investigate whether iron mass induces HO-1 overexpression and explore the role of HO-1 in rat intracerebral hemorrhage(ICH). Methods In this study,144 hydrated chloride aldehyde-anesthetized Sprague- Dawley rats were used,autologous blood were injected into the right caudate nucleus to establish the ICH model.Saline injection and health were served as controls.Deferoxamine(DFO)with an intraperitoneal injection served as intervention group.Enhanced Perl's reaction was used for iron staining and brain iron deposits were determined.Brain HO-1 level were examined by immunohistochemical analysis and reverse transcription polymerase chain reaction(RT-PCR). Results There was a 21-fold increase in iron deposits around the hematoma 7 days after the infusion of 100 μl of autologous blood.Markedly increased levels of perihematomal HO-1 immunoreactivity and HO-1 mRNA in all ICH rats were detected at 3-14 days.The addition of DFO significantly reduced iron deposits in the ipsilateral basal ganglia at 7-14 days after ICH.DFO also inhibited HO-1 overexpression at day 7,14.Correlations test showed that there were positive correlations of iron sediments with HO-1mRNA(r=0.647)and HO-1 immunopositive cells(r=0.209). Conclusions ICH causes iron accumulation in the brain.Iron overloading may induce HO-1 upregulation after ICH.Ratherly,the HO-1 moderate increasing possibly fits with the events,whereas HO-1 overexpression may result in its dysfunction.It may be prudent to intervene ICH with HO-1 inhibitor.
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BACKGROUND: It is manifested in epidemiology and clinical observation that lipoprotein (a) is a new risk factor of cerebrovascular disease and is closely related to cerebral ischemic stroke.OBJECTIVE: To discuss the relationship between levels of high serum lipoprotein (a) and stroke.DESIGN: Case controlled analysis.SETTING: Neurological Institute of Xiangya Hospital of Central South University.METHODS: Totally 294 patients with stroke were selected from Neurological Department of Xiangya Hospital of Central So, uth University between September 1999 and March 2002. Of them, 159 cases were regarded as cerebral infarction group and other 135 cases as acute hypertensive cerebral hemorrhage group. In cerebral infarction group, 109 patients had atherosclerotic cerebral infarction and 50 patients had lacunar cerebral infarction, and 94patients with contimuous health examination were regarded as health examination group. Serum lipoprotein (a) in each group was assayed with "sandwich enzyme-linked immuno-sorbent assay". According to whether the value of lipid was normal or not, patients with atherosclerotic cerebral infarction and acute hypertensive cerebral hemorrhage were divided into two groups. Comparisons between the two groups were assayed with single sample t test, and multiple liner regression was used to assay whether sex, hypertension and value of lipid were related to the level of serum lipoprotein (a).MAIN OUTCOME MEASURES: ① Comparisons of serum lipoprotein (a)among atherosclerotic cerebral infarction group, lacunar cerebral infarction group, acute hypertensive cerebral hemorrhage group and health examination group. ② Correlated analysis between serum lipoprotein (a) and lipid.RESULTS: Among 294 patients, 94 cases in control group entered the final analysis. ① Comparisons of serum lipoprotein (a) among atherosclerotic cerebral infarction group, lacunar cerebral infarction group, acute hypertensive cerebral hemorrhage group and health examination group: Levels of serum lipoprotein (a) in atherosclerotic cerebral infarction group and cerebral hemorrhage group were higher than those in health control group (P < 0.05), and concentration of lipoprotein (a) in atheroosclerotic cerebral infarction group was increased as compared with that in acute hypertensive cerebral hemorrhage group (P < 0.05). Also, level of lipoprotein (a) in lacunar cerebral infarction group was a little higher than that in control group,but the difference was not significant (P > 0.05). ② Correlated analysis between serum lipoprotein (a) and lipid: Levels of lipoprotein (a) in both normal lipid group and abnormal lipid group were assayed with single sample t test, and the results showed that levels in the two groups were similar (P > 0.05). Multiple liner regression was used to assay whether sex,hypertension and value of lipid were related to level of serum lipoprotein (a).CONCLUSION: Levels of lipoprotein (a) may be an independent risk factor for cerebral hemorrhage and atherosclerotic cerebral infarction.
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BACKGROUND: Alginic sodium diester (ASD) possesses neuroprotective function because of its selective calcium antagonist effects.OBJECTIVE: To compare the influences of ASD on intraneuronal Ca2+content and nerve cell apoptosis before and after reperfusion in focal cerebral ischemic rats.DESIGN: Randomized controlled observation.SETTING: Neurological Department of Xiangya Hospital Affiliated to South China University; Laser Orthopedic Surgery of the First Hospital Affiliated to Southern China University.MATERIALS: This experiment was carried out between November 2003and April 2004 at the Neurological Department of Xiangya Hospital Affiliated to South China University. A total of 65 male SD rats were recruited and randomized into 6 groups; 17 got lost during the experiment, and the other 48 rats completed the experiment with 8 rats in each group.METHODS: In sham operation group, an incision was made on rats' cervical skin and sutured. Right cerebral middle artery was occluded in rats of ischemic group, ASD 5 mg/kg preischemic group, ASD 5 mg/kg postischemic group, ASD 10 mg/kg preischemic group, and ASD 10 mg/kg postischemic group. After that, rats in all but ischemic group were subjected to intraperitoneal injection of various dosage of ASD or excipient 30minutes before reperfusion and 5 hours after reperfusion. FCM was used to determine intraneuronal Ca2+ content and rate of nerve cell apoptosis;meanwhile, neurological dysfunction was scored.MAIN OUTCOME MEASURES: [1] Influence of ASD on the score for neurological dysfunction, intraneuronal Ca2+ fluorescence intensity, and neuronal apoptosis in rats with right cerebral middle artery ischemia. [2]Correlation of behavioral obstacle score with intraneuronal Ca2+ fluorescence intensity and neuronal apoptosis in rats with right cerebral middle artery ischemia.RESULTS: Totally 65 rats were enrolled in this study, 17 of which got lost and the other 48 rats entered the result analysis. [1] Influence of ASD on the score for neurological dysfunction, intraneuronal Ca2+ fluorescence intensity, and neuronal apoptosis in rats with right cerebral middle artery ischemia: The score was obviously reduced in ASD 5 mg/kg preischemic group, ASD 5 mg/kg postischemic group, ASD 10 mg/kg preischemic group and ASD 10 mg/kg postischemic group as compared with ischemic group (1.80±0.21, 2.20±0.23, 1.20±0.11, 2.00±0.22, 3.40±0.65); moreover,functional improvement was more obvious due to pre-reperfusional administration than post-reperfusional administration. Intraneuronal Ca2+ concentration was reduced after ASD administration at different degrees and lower than that of ischemic group. Decrement of intraneuronal Ca2+ concentration was found most obvious due to 10 mg/kg ASD administration 30 minutes before reperfusion, approximately reduced by 70%; moreover, neuronal apoptosis rate on the ischemic side was obviously suppressed by ASD administration, displaying time-dependent manner, with apoptotic suppression effect more obvious in pre-reperfusional group than in post-reperfusional group (5.68%, 10.03%; 4.00%, 9.91%). [2] Correlation of behavioral obstacle score of right cerebral middle artery ischemic rats with intraneuronal Ca2+ fluorescence intensity and membrane associated protein/propidium iodide apoptosis: Obvious positive correlation was found between behavioral obstacle score and intraneuronal Ca2+ fluorescence intensity and detection rate of membrane associated protein/propidium iodide apoptosis (r=0.51,0.62, P < 0.05); intraneuronal Ca2+ fluorescence intensity was also positively correlated with the detection rate of membrane associated protein/propidium iodide apoptosis (r=0.84, P < 0.05).CONCLUSION: [1] ASD can exert anti-apoptosis effect by suppressing the increment of intraneuronal Ca2+ concentration, thus having neuroprotective function and ultimately improving neurological dysfunction. [2] Its effect displays time-dependent manner, and neurological functional improvement is more obvious by pre-reperfusional administration than by post-operational administration.
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<p><b>OBJECTIVE</b>To study the characteristic of the mutation of neurofilament-light (NF-L) gene in Chinese Charcot-Marie-Tooth disease (CMT) patients.</p><p><b>METHODS</b>Mutation analysis of NF-L gene was made by use of polymerase chain reaction-single strand conformation polymorphsim combined with DNA direct sequencing in 32 CMT probands from the Hans of five provinces in China who had been diagnosed by clinical feature and electromyography and/or biopsy of sural nerve.</p><p><b>RESULTS</b>In 32 CMT probands, only one sporadic case was found to display variant banding pattern, and this case was confirmed as 1329C to T (Tyr443Tyr) single nucleotide polymorphism by sequencing.</p><p><b>CONCLUSION</b>Mutation of NF-L gene may be rare in Chinese CMT patients.</p>
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Adolescent , Adulte , Enfant , Enfant d'âge préscolaire , Femelle , Humains , Mâle , Adulte d'âge moyen , Séquence nucléotidique , Maladie de Charcot-Marie-Tooth , Génétique , Chine , ADN , Chimie , Génétique , Analyse de mutations d'ADN , Données de séquences moléculaires , Mutation , Protéines neurofilamenteuses , Génétique , Mutation ponctuelle , Polymorphisme de conformation simple brinRésumé
<p><b>OBJECTIVE</b>To investigate the relationship between G1025C (Try316Ser) polymorphism in exon 8 of apolipoprotein H (apoH) gene and stroke and to evaluate the effect of G1025C(Try316Ser) polymorphism on plasma lipid levels in Changsha Hans.</p><p><b>METHODS</b>G1025C (Try316Ser) polymorphism in apoH gene was determined by PCR-single strand conformation polymorphism analysis and DNA sequencing in 100 healthy controls, 260 patients with stroke, and 20 stroke pedigrees. Serum antiphospholipid antibody (APA) levels were tested by enzyme linked immunosorbent assay (ELISA). Plasma lipid levels were measured by routine methods.</p><p><b>RESULTS</b>No statistically significant differences were found in frequencies of genotypes and alleles of G1025C (Try316Ser) polymorphism between the controls and stroke patients. The serum levels of TG in the GC genotype of cerebral infarction patients and controls were markedly higher than those in GG genotype.</p><p><b>CONCLUSION</b>There was no association betweenG1025C (Try316Ser) polymorphism and stroke in Changsha Hans. G1025C (Try316Ser) polymorphism was associated with plasma lipid metabolism in Changsha Hans.</p>