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Objective To investigate the effect of doxycycline on the Th1/Th2 cell balance in experimental allergic encepha-lomyelitis(EAE)rats.Methods Forty female Wistar rats were randomly divided into the EAE control group,low,medium and high does DOX treatment groups,10 cases in each group.The onset situation in rats was observed.The IL-4 and IFN-γlevels secreted by peripheral blood mononuclear cells (PBMC)at the peak stage were detected.The levels of IL-1β,IL-10,TNF-αin brain tissue,and the albumin content in cerebrospinal fluid and serum were detected.The QA value was calculated.Results In each DOX group,the clinical symptoms of rats were alleviated compared with the EAE control group.In each DOX group,the PBMC secreting IFN-γlev-el and IFN-γ/IL-4 ratio in the onset peak stage were lower than those in the EAE control group,while the IL-4 level was higher than that in the EAE control group(P 0.05),but the difference between other DOX groups had statistical significance(P <0.01).The IL-1βand TNF-αlevels of brain tissue and QA value during onset peak stage in various doses DOX groups were decreased compared with the EAE control group,while the IL-10 level was increased compared with the EAE control group(P <0.05).With the DOX dose increasing,the levels of IL-1β,TNF-αand QA value in various doses DOX groups became lower,the IL-10 level became high-er,there was statistically significant difference among various doses DOX groups (P <0.05 ).Conclusion DOX can obviously alle-viate the clinical symptoms of EAE rats,its mechanism may be related with that DOX could decrease the level of Th1 cytokine and increase the level of Th2 cytokine,correct the Th1/Th2 cell balance,thus protect the blood brain barrier(BBB).
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Objective To explore the appropriate dosage of drugs inducing experimental allergic en cephalomyelitis (EAE) in mice,and evaluate the modified model mice.Methods Different doses of myelin oligodendrocyte glycoprotein (MOG35-55:200 μg,100 μg,50 μg,25 μg),together with different doses of inactivation of mycobacterium tuberculosis (H37RA:800 μg,250 μg,100 μg) and pertussis toxin (500 ng,200 ng),were used to induce the EAE model.After immunized,the clinical disease severity of EAE mice was measured by the standard EAE grading clinical score daily.The open field test was used to detect the locomotion of mice.The Western blot and immunofluorescence were used to detect the level of myelin basic proteins (MBP) in different brain regions of mice.Results Compared with the EAE mice induced with high-dose drugs,the mice with low-dose drugs (25 μg MOG35-55,100 μg H37RA,200 ng pertussis toxin) had low neu rological scores.And they displayed normal locomotion compared with the control mice (day 16:group EAE (8.885±0.772) cm/s vs control group (8.933±0.567) cm/s,P＞0.05;day 31:group EAE (11.130±0.630) cm/s vs control group (10.670±0.959) cm/s,P＞0.05;day 55:group EAE (7.686±0.428) cm/s vs control group (8.313±0.918) cm/s,P＞0.05).Moreover,there was a significant decrease of MBP in the parahippocampal cortex (PHC) and fimbria-fornix of EAE mice induced with low-dose of drugs (PHC:group EAE (0.369±0.096) vs control group (1.000±0.163),P＜0.05;fimbria-fomix:group EAE (0.494±0.071) vs control group (1.000±0.143),P＜0.05).Conclusion The EAE mice induced with low-dose drugs(25 μg MOG35-55,100 μg H37RA,200 ng pertussis toxin) have low neurological scores,normal locomotion,and myelin impairment in the central neuronal system.And it can be used in the cognitive behavioral research of demyelination disease,such as multiple sclerosis.
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Objective To investigate immunological mechanism underlying leflunomide ( LEF ) against experimental allergic encephalomyelitis ( EAE) by studying the effects of LEF on peripheral blood CD28/CTLA-4 costimulatory molecules expression in guinea pig with EAE.Methods 50 adult female guinea pigs were randomly divided into normal control group,low dose group,EAE control group,middle dose group,and high dose group, 10 guinea pigs in each group respectively.Low, medium and high dose group were treated with LEF 10 mg/kg· D, 20 mg/kg· D and 40 mg/kg· D orally, 1 times/day, to the termination of the experiment.The expression of CD28, CTLA-4 were detected by flow cytometry, incidence was recorded at the same time.Results Compared with EAE control group,high dose and middle dose group incubation period were prolonged, progress period were shorten and neurological dysfunction score decreased(P<0.05).Compared with normal control group, the expression of CD28 of EAE control group increased and the decreased expression of CTLA-4 (P<0.05).High, middle dose treatment group compared with EAE control group CD28 down regulated expression (P<0.05), but the expression of CTLA-4 increased(P<0.05).Among the treatment groups, of CD28 molecules with high dose group decreased significantly(P<0.05), the expression of CTLA-4 molecules with high dose treatment groups upregulated significantly (P<0.05).Correlation analysis showed that the EAE control group, the treatment group the CD28/CTLA-4 ratio in peripheral blood and nerve dysfunction score is proportional ( r=0.85, P=0.002; r=0.77, P=0.000).Conclusion LEF can reduce EAE guinea pig neurological symptoms, the better and the higher dose effect.Its mechanism may be through down-regulation of CD28 molecules in peripheral blood, upregulation of the expression of CTLA-4 molecule.so as to reduce the inflammatory response, relieve the clinical symptoms.
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Objective To investigate the effects of ulinastatin(UTI)on the nerve regeneration of mice experimental allergic encephalomyelitis and the expression of related factors and protein.Methods Forty mice were randomly divided into four groups:ulinastatin group(U),atorvastatin group(A), empty control group(C)and normal control group(N).The experimental autoimmune encephalomyelitis(EAE)in mice was constructed by Freund's complete adjuvant and MOG35-55 polypeptide.Histopathological changes were observed by HE,LFB and Bielschowsky stained at the 3rd week and 4th week after immunized of each group.The expressions of CD4 +T cells were estimated by immunohistochemical method.The expression of myelin basic protein (MBP),brain-derived neurotrophic factor(BDNF),growth associated protein-43(GAP-43),2',3'-cyclic nucleotide-3'-phosphodiesterase(CNP)were detected by Western-blot.Results The largest neurological score of group U was lower than group C,and the difference was statistically significant(P<0.05 ).Pathological features showed that the inflammatory cells,demyelination of spinal cord and axonal injury of group U were lighter than group C.With the duration of treatment,nerve injury decreased.After UTI treatment,the expression of MBP,BDNF,GAP-43,CNP increased.They were statistically significant difference when compared with group C(P<0.05).There was no significant difference between ulinastatin and atorvastatin in the treatment of EAE.Conclusion Ulinastatin could reduce the extent of nerve damage effectively and promote its regeneration which provide a theoretical basis for the clinical treatment of MS.
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Background Optic neuritis is closely associated with multiple sclerosis (MS).Its pathogenesis is uncompletely clear,and less basic researches are carried out at home and abroad. Objective This study was to reveal the expression of myelin basic protein (MBP) in the optic nerve of rat with experimental allergic encephalomyelitis (EAE) and to provide a theoretical evidence for the research of the relationship of optic neuritis with MS. Methods Fifty clean Wistar rats were randomized into the control group and immune 8,12,18 and 25 days groups.Myelencephalon was collected from 5 guinea pigs to prepare the homogenate and mixed with the isovolumetric complete Freud' s adjuvant (CFA).The 0.5 ml mixed antigen emulsifier was subcutancously injected into the 4 maps together with Bordetella pertussis 0.2 ml under the cutancous of dorsalis pedis at 0 and 48 hours to induce the EAE.Behavior of the rats was evaluated to score the neurological function.The optical nerve sections were prepared 8,12,18 and 25 days after immunology for the histopathological examination,and immunochemistry and Western blot were used to detect the expression of MBP in optic nerve.The use of the animals complied with the Regulation for the Administration of Affairs Concerning Experimental Animals by State Science and Technology Commission. Results The disorder of motor nerve was seen 12 days following the immune,and the clinical neural functional scores were significantly higher 12 day and peaked on 18 days myelination and then gradually reduced.The histopathological examination showed that the irregular alignment of neural fiber was found at 12 days,and changes of cellular structure,edema of neural shaft bunch were observed at 18 days.However,the abnormal cells were significantly less 25 days following the immune.Immunochemistry showed that the MBP was expressed mainly in the myelination of optic nerve fibers.The numbers of positive cells for MBP were (115.75±26.49)cells/5 fields at the 12th day,showing a significant lowing in comparison with (167.44±22.49)cells/5 fields of control group (t=4.537,P＜0.05 ).The positive cells were lest at the 18th day with the values ( 75.57 ± 34.54) cells/5 fields ( t =6.362,P＜0.01 ).At the 25th day,positive cells increased to ( 117.63 ± 13.78) cells/5 fields,which still was lower than those of the control group ( t =4.068,P＜0.05 ).Western blot assay illuminated that with the prolong of immune time,MBP/β-actin ratio in optic nerve was gradually reduced and followed the same pattern at the 12th day( t =4.639,P＜0.05 ).At 18 days after immune in comparison with the control group,the expression of MBP/β-actin ratio in optic nerve was the least (t=8.427,P＜0.01). Conclusions MBP can be degraded in rat optic nerve.This is a further evidence that optic neuritis is a severe demyelination disease.It is clearly related to MS.
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Objective To investigate the effect of L-selectin in experimental allergic encephalomyelitis (EAE) of Wistar rats.Methods The rats were randomly divided into four groups;the normal group,the CFA group, the LMS group and the model group;The animal models were established in rats by immunization with myelin basic protein of spinal cord of guinea pig and complete Freund's adjuvant(CFA).The symptom of EAE was observed; pathological feature and myelin of brain and spinal were detected with HE stain and Loyez's stain respectively.The number of positive vessels of L-selectin expression was detected by immunohistochemistry.Results 100% experimental Wistar rats treated with MBP and levamisole developed EAE,but none of the other groups.The number of positive vessels of L-selectin expression was (31.86 ± 1.39) in model group, obviously higher than that of in the normal group (1.38 ±0.18) ,the CFA group( 1.50 ±0.27) and the LMS group(7.25 ±0.59) (all P <0.05) ;The inflammation cells were found around vessels and demyelination were seen in white matter of brain and spinal cords.Conclusion The expression of L-selectin should play an important role in EAE.
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Objective:To investigate the beneficial effect of erythropoietin(EPO)on experimental allergic encephalomyelitis(EAE).Methods: The severity of EAE mice with or without EPO therapy were evaluated through clinical symptoms score and histological observation.Mononuclear cells from spleens,lymph nodes, brains and lumber spinal cords were applied to flow cytometry to detect ratios of CD4~+T subgroup, scales of apoptotic and dead cells, levels of inflammatory cytokines.LDH release of peripheral mononuclear cells were examined after incubating with EPO at different concentrations.Results: EPO ameliorated clinical symptoms and infiltration of pathological inflammatory cells in EAE mice(P＜0.05); Ratio of CD4~+T subgroup, levels of IL-17 and IFN-γ in EAE mice with EPO therapy were significantly lower than those of EAE control group(P＜0.05).No statistical significant differences existed on scales of dead cells, levels of IL-10 and CD4~+ CD25~+ T cells (P＞0.05).EPO at the concentrstions of 1-1 000 U/ml had no effect on LDH release of peripheral mononuclear cells(P＞0.05).Conclusion: EPO play the role of neuroprotecion in EAE mice by the way of decreasing infiltrating inflammatory cells and lowering the levels of IL-17 and IFN-γ.
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Objective To induce experimental allergic encephalomyelitis (EAE) in female C57BL/6 mice with the extracellular domain of myelin oligedendroglia glycoprotein(MOG~(Igd)). Percentages of CD4~+ CD25~+ T cell (Tr) were tested , and also normalized expressions of Foxp3. Methods Molecular cloning technology was used to produce MOG~(Igd) fusion protein. The MOG~(Igd)-TrxA fusion protein and TrxA protein were purified by metal chelate affinity chromatography (MCAC). Mice were injected s. c. in the flank with 300 μg MOG~(Igd) in complete Frcund's adjuvant (CFA) supplemented with 4 μg/μl Mycobacterium tuberculosis. H37Rv. Mice received 0.4 ml emulsion of spinal cord homogenate of guinea pigs (GPSCH) in positive control group, and the same volume emulsiom of TrxA in negative control group, while mice served as normal control received only saline/adjuvant. Mice were monitored two times a day for continuously 30 days by double bind. Clinical scores and histopathology were evaluated. Then, mice were sacrificed. The spinal cord and brain were removed and fixed in buffered formalin. Horizontal sections taken from the central nervous system(CNS) were stained with haematoxylin and eosin (HE), and Kluver-Barrera staining. Also, immunohistochemistry was performed. Percentages of CD4~+ CD25~+ T cells were tested through flow cytometric analysis, and real-time PCR was performed to test normalized expressions of Foxp3 mRNA. Then, correlations between the two were performanced. Results Mice in both MOG group and GPSCH group shew chronic non-remitting course. The onset of disease, time when the most severe clinical symptoms happened and the clinical score between the two groups shew no significant differnces (P>0.05). However, neither in TrxA treated group nor in normal control group did animals exhibit clinical signs of EAE. Histologic sections of the brain and spinal cord taken from affected animals shew perivascular infiltration of mononuclear cells, gliosis, and multifocal demyelination. Lesions scattered throughout the CNS including brainstem, spinal cord, cerebellum, and penventricular white matter. There were significant differences between MOG group and TrxA group in the level of lesion-ceutric AQP-4 expression showing up by immunohistochemistry (P<0.05). Percentages of CD4~+ CD25~+ T cells in MOG group and GPSCH group were (4.71±1.61) % and (1.44±0.65) %, respectively, both of which were significantly lower than those in the normal control group or TrxA treated group (P<0.01). And the difference between MOG group and GPSCH group also reached statistics meaning (P<0.01). Normalized expression of Foxp3 mRNA in MOG group was 2.26± 1.97, and was not significantly higher than the 1.44±1.20 level in GPSCH group (P>0.05). However, they beth were statistically lower than that in the negative control group, namely 8.58±3.34 (P<0.01). Percentages of CD4~+ CD25~+ T cells was statistically correlated with expressions of Foxp3 mRNA (P< 0.05). Conclusion EAE induced in C57BL/6 mice with MOG~(Igd) is reproduceable. It shares the similar clinial signs and pathologic features with human multiple sclerosis(MS). Thus, we find a good way to further study the immune mechanisms of MS and also to search for the effective treatments.
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Objective To study the role of Schwann cells apoptosis in the pathogenesis of experimental autoimmune neuritis(EAN) in TNF receptor Ⅰ knock out(TNFR Ⅰ-/-)mice.Methods For induction of EAN,TNFRⅠ-/- and wild type C57BL/6 mice were immunized by subcutaneous injection into the back with the peripheral nerve P0 protein peptide 180-199;clinical scores of EAN were assessed and scored immediately before immunization(day 0) and thereafter every other day until day 46 post immunization(p.i.).On day 22 p.i.,Schwann cells were collected from the two groups and cultivated in vitro.The expressions of Fas and Annexin-Ⅴ(Annexin-Ⅴ+/PI-)on Schwann cells from TNFRⅠ-/-and wild type EAN were detected by flow cytometry.Results More light clinical signs of EAN were observed in the TNFRⅠ-/-mice(1.50?0.19) than in wild type mice(1.90?0.16);the percentage of Fas expression on Schwann cells was significantly decreased in TNFRⅠ-/-mice(88.03%?1.40%)as compared with wild type mice(94.70%?1.53%)(P
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Objective To investigate the effects of prednisone(PRD) on experimental allergic encephalomyelitis(EAE) and the mechanism.Methods Lewis rats were injected with mixture of guinea pig spinal extracts and Freund's adjuvant(FA) to induce EAE.PRD(5 mg/kg) was orally given ten days after the injection.The clinical manifestation of rats,their peripheral blood lymphocytes CD3~(+),CD4~(+),CD8~(+) and NK subsets,and pathology changes of brain and spinal were studied on day 26.Results In model CD3~(+) ratio is 63.2%,CD4~(+)ratio 46.8%,CD8~(+)ratio 17.4% and NK ratio 10.2%.In PRD CD3~(+) ratio is 69.5%,CD4~(+)ratio 51.8%,CD8~(+)ratio 18.1% and NK ratio 5.3%.PRD obviously decreased the clinical scores of EAE rats and peripheral blood NK ratio,increased CD3~(+) and CD4~(+)ratio,inhibited brain inflammatory reaction and demyelination.However,PRD didn't affect peripheral blood lymphocytes CD8~(+) and CD4~(+)/CD8~(+)ratio.Conclusions PRD is effective in the treatment of EAE rats,and the therapeutic mechanism may be contributed to the decrease of the peripheral blood NK ratio and increase CD3~(+) and CD4~(+)ratio.
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Experimental allergic encephalomyelitis (EAE) lesions by autoimmune inflammatory mechanism are characterized by the activation of microglia and astrocytes during the peak symptomatic stage of the disease. Besides it is well known that ROS and nitric oxide (NO), which is come out from activated inflammatory cells, play important role in the pathogenesis of EAE lesions. And vitamin C (L-ascorbic acid), which may protect from the deleterious effect by reducing iron (Fe2+) or copper (Cu2+) ions and maintain tissue homeostasis by removing of oxygen free radical, is inevitable to help many enzymatic reactions of cells. Previous report already investigated expression and functional analysis on various vitamin C transporters of vitamin C in many cell types. However, the researches for the vitamin C transporters are mostly performed in the normal state but not disease model yet. Therefore, for the first time, we investigated to know whether the SVCT1, 2 immunoreactivity may be observed in the astrocyte of EAE rat spinal cord. In the comparison of control and peak time group, the number of SVCT1, 2 immunoreactive cell was inclined to increase (P<0.05) as respectively 100+/-29.93, 135+/-34.62 in the control group, and 179+/-54.29, 349+/-73.56 in the peak time group. SVCT2 immunoreactivity was not doubly colocalized with GFAP antibody in the control group. In contrast, the astrocytes of the peak time group showed SVCT2 immunoreactivity in the perivascualr region and the cell number of doubly (SVCT2, GFAP) colocalized was 15+/-5.67 (P<0.05). We are firstly demonstrated that, in the evolving processes of EAE, astrocytes are able to use the vitamin C via the SVCT2. Taken all findings into consideration, the present data on the typical anti-oxidant vitamin C and its transporters, which may play a role in removing ROS, could be considered as a target to the therapeutic strategy of EAE and is also very useful to identify the characterization of vitamin C in the biological organism.
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Animals , Rats , Ascorbic Acid , Astrocytes , Cell Count , Copper , Encephalomyelitis, Autoimmune, Experimental , Homeostasis , Ions , Iron , Microglia , Nitric Oxide , Oxygen , Spinal CordABSTRACT
Objective To establish the animal model of experimental allergic encephalomyelitis(EAE)in Lewis rats.Methods The EAE was induced by giving hypodermal injections in feet with spinal cords homogenate of guinea pigs(GPSCH)and complete Freund's adjuvant(CFA)containing 8mg.ml-1 bacille calmette guerin(BCG).The EAE model was evaluated by clinical manifestations and pathologic findings which was studied with the aid of light and electron microscope.Results The EAE in Lewis rats had an incidence of 9/10,a latency of 12.6?1.01d.Bordetella pertussis vaccine(BPV)could increase the morbidity,shorten the latency(P
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Objective To establish the model of P2 peptide-induced experimental autoimmune neuritis(EAN)in rats and explore the roles of Th_1/Th_2 type eytokines in EAN.Methods Lewis rats were grouped into EAN rats and control rats.The EAN rats were immunized by injection into both hind footpads of inoculums containing 100 ?g or 200 ?g of P2_(57-81)peptide and FCA while the control rats were immunized with FCA only.Clinical scores were compared at the maximum of disease.Supernatant productions of IFN- ?, IL-4 and IL-10 secreted by lymphocytes and obtained on day 14 after the immunization were examined. Histopathological assessment of sciatic nerves was made.Results Peak clinical scores of P2_(57-81)200 ?g (3.6?0.3)group were significantly higher than P2_(57-81)100 ?g group(2.2?0.6,P
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Objective To establish P2 or P0 peptide-induced experimental autoimmune neuritis (EAN)in the Lewis rats and to explore the optimal type and doses of antigen inoculated to induce EAN and the associated cell-mediated immune mechanisms.Methods Lewis rats were classified into EAN and control groups.The EAN rats were immunized by injection into both hind footpads of inoculums containing 100 or 200 ?g of P2_(57-81)peptide or 200?g of P0_(180-199)peptide and Freund's complete adjuvant(FCA),and the control rats were immunized with FCA only.Clinical scores were compared when they were at peak time of paralysis.Lymphocyte proliferation assay,the ratio of CD_4~+ T cells to lymphatic monocytes and percentage of CD_4~+ CD_(25)~+ T cells to CD_4~+ T cells obtained on day 14 post-immunization were examined.Histopathalogical assessment of sciatic nerves was made.Results Peak clinical scores of P2_(57-81)200 ?g group were dramatically higher than those in P2_(57-81)100 ?g group and P0_(180-199)200 ?g group(both P
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Objective To observe the time interval changes of the expression of Nogo-A in the intumescentia lumbalis of rats with experimental allergic encephalomyelitis(EAE),and explore the function of Nogo-A in the happening and development of EAE.Methods One hundred and six Wistar rats(female) were randomly divided into 2 groups:EAE group(70 rats)and control group(36 rats).Female Wistar rats were used to make EAE animal models,immunized by fresh cavia cobaya spinal cord homogenate and complete Freund adjuvant(CFA),at the same time,their blood brain barrier permeability was lifted by using pertussis stock solution.The rats those were coincident with the standard of being picked up were divided into 6 groups randomly according to the time of falling ill.In control group,fresh guinea pig spinal cord homogenate was replaced by sodium chloride,and rats were also divided into 6 groups randomly.Immunohistochemistry SP was used to detect expression of Nogo-A.Amyelination was detected by improved acid fuchsin and azulin myelin staining.Results In the control group,differences of Nogo-A expression in the intumescentia lumbalis were not obvious in each time group.In the EAE group,expression of Nogo-A could be observed in each time group,but their quantities were very different in contrast with those in the control group.One day after the rats had clinic symptoms,the expression of Nogo-A decreased to some extent;the third day,it reached the lowest point,and was significantly lower than that in control group(P
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Objective To study the relationship between chemokines monocyte chemoattractant protein-1(MCP-1),reduced upon activation of normal T cell expressed and secreted chemokine(RANTES) and experimental allergic neuritis(EAN).Methods EAN models were induced in Wistar rats by immunization with rabbit sciatic nerves homogenate and complete Freund's adjuvant(CFA).Expressions of MCP-1,RANTES in the sciatic nerves of experimental rats were detected by immunohistochemistry technology at different time.Results The maximum MCP-1 positive cells in the sciatic nerves were detected at 9th d.The expression of MCP-1 in EAN group was obviously higher than that in control group at 9th,15th and 21th d(all(P
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Objective:To investigate pathological changes and the expression of the matrix metalloproteinases in rat EAE.Methods:The pathological changes of EAE were studied in Wistar rat with the aid of light and electron microscope and the expression and distribution of MMP-2,MMP-9 in different tissues were detected with the method of immunohistochemistry.Results:Light microscopy showed inflammatory cuff around small blood vessels were evident, disintegration and disappear of myelin sheath were observed. Electron microscopy showed a lot of loose and fragmental spiremes of myelin sheath, the component of axons and nissl bodies in neurons were disappeared. MMP-2,-9 were expressed intensively in vascular endothelial cells, meninges and accumulative inflammatory cells.Conclusion:MMPs take the roles in every aspect of the pathological changes in EAE, it can destroy the blood brain-barrier, degrade the myeline sheath, damage the axons and generate immunogens.
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Objective To investigate which subfamily genes of T cell receptor (TCR) V? expand predominantly during the course of experimental allergic neuritis (EAN). Methods Using RT-PCR and in situ hybridization techniques,the expression levels of TCR V? 2,6,8,10,14 in the peripheral blood,lymph nodes,peripheral nerves of group EAN and those of the control group were compared. Results In group EAN,the expression of TCR V? 6?8 mRNA increased at the early phage(41.1?1.1 and 74.4?1.9 vs 25.9?1.5 and 26.1?1.6) and became more significantly at the peak of the disease,and resolved to normal at the recovery phage in the lymph nodes.But they amounted up gradually from the early stage to the peak,and then decreased a little in the infiltrating T-lymphocytes in peripheral nerves,the difference was significant.In addition,the expression of TCR V? 8 was notably higher than that of TCR V? 6 in the levels of mRNA. Conclusion The subfamilies of TCRV? genes which restrict the development of EAN due to recognizing the specific antigens are TCRV? 8 and TCRV? 6. T lymphocytes specifically expressing TCR V?6?8 genes are activated and clonally proliferated in the lymph nodes,and then migrate to the involved peripheral nerves,which might induce a series of immune lesions consequently.
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Objective To observe the effect of neuropeptide Y(NPY) on the levels of serum interleukins(ILs)in guinea pigs with experimental allergic encephalomyelitis(EAE).Methods 30 guinea pigs were divided randomly into normol control group,EAE group and NPY group.The NPY was injected into the intracerebroventricular in NPY group one week before the EAE model be made.The EAE molders were made by injecting the homogenate of rat's spinal cord into the plantar of guinea pigs in groups EAE and NPY.Then,the neurological deficits score was observed everyday,the incidence and the delitescence of EAE were observed too.The levels of serum IL-1?,IL-2,IL-4,IL-6 and IL-8 were detected,and the neuropathological examination was used when symotoms peak period of EAE models.Results(1)The incidences of the EAE in groups EAE and NPY were 100% and 90%,the delitescences of EAE were(10.0?4.8)d and(25.4?12.6)d,the neurological deficits scores at the symotoms peak period were(3.60?0.52) and(1.80?1.14),respectively.There were significantly differences between the two groups(all P
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Objective:The experimental allergic encephalomyelitis(EAE) is the most suitable animal model for investigation in the pathogenesis and the treatment of EAE.The expressions of ICAM-1,VCAM-1 in Wistar rat brain of acute EAE were investigated to study the mechanism and significance of their expressions in EAE rat brain.Methods:All experimental Wistar rats were inoculated intradermally in feet with emulsion contained guinea pig spinal cord homogenate and complete Freund’s adjuvant.The clinical manifestation and the pathological changes were observed with the aid of light and electron microscope to check the successful establishment of the model.The expressions of ICAM-1 and VCAM-1 were detected by the method of immunohistochemisty.The results of their expressions were compared by T test with controls.Results:Significant difference was found between the experimental group and the controul group in the expressions of ICAM-1 and VCAM-1 ( P