Semaphorin 3A controls allergic and inflammatory responses in experimental allergic conjunctivitis

AIM: To assess the efficacy of topical Semaphorin 3A(SEMA3A) in the treatment of allergic conjunctivitis.METHODS: Experimental allergic conjunctivitis(EAC)mice model induced by short ragweed pollen(SRW) in 4-week-old of BALB/c mice, mice were evaluated using haematoxylin and eosin(H&E) staining, immunofluor-escence and light microscope photographs. Early phase took the samples in 24 h after instillation and late phase took the samples between 4 to 14 d after the start of treatment. The study use of topical SEMA3A(10 U, 100 U,1000 U) eye drops and subconjunctival injection of SEMA3 A with same concentration. For comparison, five types of allergy eyedrops were quantified using clinical characteristics.· RESULTS: Clinical score of composite ocular symptoms of the mice treated with SEMA3 A were significantly decreased both in the immediate phase and the late phase compared to those treated with commercial ophthalmic formulations and non-treatment mice. SEMA3 A treatment attenuates infiltration of eosinophils entering into conjunctiva in EAC mice. The score of eosinophil infiltration in the conjunctiva of SEMA3 A 1000 U-treated group were significantly lower than low-concentration of SEMA3 A treated groups and non-treated group. SEMA3 A treatment also suppressed T-cell proliferation in vitro and decreased serum total Ig E levels in EAC mice. Moreover, treatment of SEMA3 A suppressed Th2-related cytokines(IL-5, IL-13 and IL-4)and pro-inflammatory cytokines(IFN-γ, IL-17 and TNF-α)release, but increased regulatory cytokine IL-10 concentration in the conjunctiva of EAC mice.CONCLUSION: SEMA3 A as a biological agent, showed the beneficial activity in ocular allergic processes with the less damage to the intraocular tissue. It is expected that SEMA3 A may be contributed in patients with a more severe spectrum of refractory ocular allergic diseases including allergic conjunctivitis in the near future.

Neuroprotective effects of gypenosides in experimental autoimmune optic neuritis

AIM：To determine whether gypenosides have protective effects in experimental autoimmune optic neuritis（EAON）.METHODS：Mice were randomly divided into seven groups：control group,model group,three different density gypenosides monotherapy,methylprednisolone monotherapy,combination of gypenosides and methylprednisolone group.The control group was subcutaneously injected with oil emulsion adjuvant and all other groups were subcutaneously immunized with an emulsified mixture of myelin oligodendrocyte glycoprotein（MOG） 35-55 peptide to induce EAON.Mice in the gypenosides groups were administered injections daily with three concentrations（15 mg/kg,30 mg/kg,45 mg/kg） of gypenosides respectively.Mice in the methylprednisolone group and the combination treatment group were injected daily with methylprednisolone（20 mg/kg） or methylprednisolone（20 mg/kg） ＋ gypenosides（30 mg/kg）,respectively.After MOG immunization,visual evoked potential（VEP）,optical coherence tomography（OCT）,and histopathologic examination were performed at 14,20,30,and 40 d post-inoculation（p.i.）.All results were expressed as mean±SEM.The data were evaluated by oneway ANOVA followed by Tukey or Games-Howell test.RESULTS：Compared with the control group,p2 latency was prolonged in the model group（P=0.041）.Combination treatment can alleviated the change in VEP at 20 d p.i.（P=0.012）.Average peripapillary retinal nerve fiber layer（RNFL） thickness was reduced in the model group（P= 0.000,30d;P=0.000,40d） and gypenosides treatment remarkably diminished the degree of RNFL degenerationat 30 d and 40 d p.i（P=0.000,30d;P=0.000,40d）.The pathomorphological results showed a decrease in demyelination（P=0.020） and inflammatory reactions in the combination group compared with the model group（20d p.i.）.Gypenosides treatment also alleviated the degree of axonal loss（40d p.i.）（P=0.003）.CONCLUSION：Treatment with gypenosides exerts protective effects on retinal nerve fibers and axons in EAON.When combined with gypenosides,methylprednisolone reduces demyelination in the acute stage of EAON.

Effect of olfactory ensheathing cell transplantation on myelin repair and motor function in a rat model of experimental allergic encephalomyelitis

BACKGROUND： Olfactory ensheathing cell transplantation can activate axonal regeneration and enhance myelin repair, which are beneficial for treating demyelinating diseases. OBJECTIVE： To explore the effects of olfactory ensheathing cell transplantation on myelin repair, synaptophysin expression, and motor function in a rat model of experimental allergic encephalomyelitis. DESIGN, TIME AND SETTING： A randomized, controlled experiment was performed at the Laboratory of Provincial Hospital affiliated to Shandong University between August 2006 and September 2007. MATERIALS： Dibenzylamine （Hoechst 33342）, luxol fast blue, and rabbit anti-rat synaptophysin antibody were provided by Sigma, USA. METHODS： Olfactory ensheatbing cells extracted from neonatal Wistar rats were cultured for 10-14 days and labeled with dibenzylamine. Spinal cord extracted from a healthy guinea pig was homogenized and equally mixed with complete Freund＇s adjuvant; thereafter, the mixture was intracutaneously injected into two posterior voix pedis of healthy male Wistar rats to establish models of experimental allergic encephalomyelitis. Rats were randomly divided into a control encephalomyelitis group and an olfactory ensheathing cell transplantation group, 36 rats in each group. Physiological saline （2 μ L） or an olfactory ensheathing cell suspension （2 μ L） was separately injected along lateral cerebral ventricle at day 7 post-model induction. MAIN OUTCOME MEASURES： The migration and distribution of olfactory ensheathing cells were observed under fluorescence microscopy; myelin repair was detected using hematoxylin-eosin staining and luxol fast blue staining; synaptophysin expression was measured using immunohistochemical staining; motor function was evaluated using a motor function scale. RESULTS： Olfactory ensheatbing cells could survive in vivo and migrate to the distal end of the transplant focus and spinal cord, and survived 21 days. Hematoxylin-eosin staining and luxol fast blue staining indicated that myelin in the transplantation group was intact, and the inflammatory focus gradually disappeared. Transplantation increased synaptophysin expression （P 〈 0.05 versus control） and motor function （P 〈 0.05）. CONCLUSION： Olfactory ensheathing cell transplantation can promote myelin repair, increase synaptophysin protein expression, and ameliorate motor function in a rat model of experimental allergic encephalomyelitis.

Immunity phenomena following olfactory ensheathing cell transplantation into experimental allergic encephalomyelitis rat brain

Olfactory ensheathing cells （OECs） can promote axonal regeneration and remyelination for the treatment of spinal cord injury. OECs can also treat experimental allergic encephalomyelitis （EAE）, but it remains unclear whether OECs might be rejected by the immune system in the brain including the destruction of the blood-brain barrier under inflammation, the release of inflammatory factors, the activation of local antigen-presenting cells （e.g., microglia cells） and antigen drainage. We found that OECs expressed major histocompatibility complex （MHC）-I molecules on the cell surface, barely expressed MHC-II, but MHC-II could be induced by interferon-v, suggesting that OECs have certain immunogenicity. When OECs were transplanted into normal animal brains, no OECs were phagocytosed by dendritic cells in the cervical lymph node, and OECs did not induce lymphocyte proliferation, which indicates that OECs share some immune privilege under normal conditions. However, OECs in the rat EAE brain were phagocytosed by dendritic cells in the cervical lymph node and enhanced lymphocyte proliferation. These findings suggest that OECs are rejected because of increased immunogenicity in EAE brain, and that brain inflammation, in particular activated dendritic cells, may be a prerequisite for rejecting OECs.

PD-L1 is increased in the spinal cord and infiltrating lymphocytes in experimental allergic encephalomyelitis

Experimental allergic encephalomyelitis is a mouse model of human multiple sclerosis with similar pathology and pathogenesis. Thl cells play an important role in the pathogenesis of experimental allergic encephalomyelitis. This study determined the potential effect of programmed cell death 1 ligand 1 in the pathogenesis of experimental allergic encephalomyelitis induced by injecting myelin oligodendrocyte glycoprotein, complete Freund＇s adjuvant and Bordetella pertussis toxin into C57BL/6J mice. Experimental allergic encephalomyelitis mice developed disease and showed in- flammatory changes in the central nervous system by hematoxylin-eosin staining of spinal cord pathological sections, demyelination by Luxol fast-blue staining and clinical manifestations. The expression of programmed cell death 1 ligand 1 in mice was detected by immunohistochemistry, flow cytometry and western blot anatysis. The expression of programmed cell death 1 ligand 1 in the spinal cord and splenocytes of mice was significantly increased compared with normal mice. Our findings suggest the involvement of programmed cell death 1 ligand 1 in the pathogenesis of ex- perimental allergic encephalomyelitis and suggest this should be studied in multiple sclerosis.

Treatment of rats with experimental allergic neuritis using high dose immunoglobulin

To investigate the therapeutic potential of high dose immunoglobulin (HIG) in experimental allergic neuritis (EAN) to provide a theoretical basis of its clinical use in the treatment of human inflammatory demyelinating neuropathies Methods Female Lewis rats were induced to EAN, and divided into experimental and control groups The rats were treated with either 0 3?g/kg·day 1 of IgG or an equivalent volume of 0 15?mol/L glycine Clinical, electrophysiologic, and histologic evaluations were carried out in a blind fashion Results Clinically, rats treated with IgG had significantly less severe symptoms ( P <0 001) and slower progression ( P <0 001) than controls Electrophysiologically, the mean conduction latency of the experimental group was significantly shorter than controls ( P <0 05) Histologically, rats treated with IgG prepared from normal Lewis rats had a significantly lower percentage of demyelinated fibers ( P =0 01) and total abnormal fibers ( P <0 001) than controls Statistically, clinical, electrophysiologic and morphologic data were all significantly correlated Conclusions The EAN animal model is reliable for observation of HIG effects, and useful to provide data for clinical work HIG has a significant therapeutic effect in EAN when given soon after disease onset It can reduce clinical disease severity and decrease the number of demyelinated fibers as well as the number of total abnormal fibers For the current controversy over whether HIG is effective, the results of this research support the clinical use of HIG in human demyelinating neuropathy

Tumor necrosis factor-alpha in experimental autoimmune neuritis

Tumor necrosis factor-α （TNF-α） plays a key role in the pathogenesis of experimental autoimmune neuritis （EAN） as well as Guillain-Barre syndrome. The proposed pathogenesis of TNF-α associated neuropathies involves immune-mediated attack to blood-nerve barrier, aggravated production of pro-inflammatory cytokines, and the induction of Schwann cells apoptosis. TNF-α may play a regulatory role by increasing production of interleukin-1 in macrophages, attenuating T cell receptor signaling and regulating apoptosis of potentially autoreactive T cells in EAN. The data suggest that antagonizing TNF-α functions or suppressing TNF-α production may be useful in the acute phase of EAN treatment, but further studies are required.

Effect of neuropeptide Y on white matter demyelination and serum interleukin-4 and gamma-interferon levels in the guinea pig with experimental allergic encephalomyelitis

BACKGROUND： Neuropeptide Y （NPY） may influence differentiation of Th cells immunological pathology of experimental allergic encephalomyelitis （EAE） is differentiation of Th cells It is assumed that the related to abnormal OBJECTIVE： To investigate the effect of NPY on white matter demyelination, the serum levels interleukin-4 （IL-4） and gamma-interferon （IFN-γ ）, as well as EAE pathogenesis in an EAE guinea pig model following NPY injection into the lateral cerebral ventricle. DESIGN, TIME AND SETTING： A randomized controlled animal study, which was performed in the Infection Immunity Animal Laboratory, Affiliated Hospital of Luzhou Medical College, China, from October 2005 to April 2006. MATERIALS： Thirty healthy female guinea pigs of 8-12 weeks of age, and 10 healthy female rats of three months of age were used. NPY was provided by Sigma Company, USA. NPY kit was provided by Beijing Huaying Biotechnology Institute, China. METHODS： Thirty guinea pigs were randomly divided into three groups： normal control group, EAE model group, and NPY intervention group （n =10 per group）. Normal control group and EAE model group： Saline （10μ L, once） was injected into the lateral cerebral ventricle. After one week, the same volume of Freund＇s adjuvant complete was either injected subcutaneously into two post-palms or EAE was modeled. NPY intervention group： EAE was modeled after one week and NPY was injected （10 μ L of 6 nmol NPY, once） into the lateral cerebral ventricle. Myelin basic protein （MBP） antigen made from rat spinal cord homogenate and Freund＇s adjuvant complete were injected subcutaneously into both post-palms （0.2 mL per palm） to establish the EAE model. MAIN OUTCOME MEASURES： White matter demyelination of the cerebrum, cerebellum, brain stem, and spinal cord were observed by light microscopy after HE staining. Levels of serum IFN-γ and IL-4 were detected by the double antibody sandwich ABC-ELISA technique. NPY content was detected by radioimmunoassay. RESULTS： Pathological alterations in the NPY intervention groups were reduced compared to those in the EAE model group, suggesting a reduction and remission of white matter demyelination with NPY treatment. When compared to the model group, the serum IL-4 level was increased in the NPY intervention group during the high-frequent EAE stage （P 〈 0.01）, but the serum IFN-γ level was decreased （P 〈 0.01）. Furthermore, the EAE latency was prolonged （P 〈 0.01）, the neurological scores were decreased in the high-frequent EAE stage （P 〈 0.01）, and the death rate was decreased （P 〈 0.05）. NPY content and the serum IL-4 level at the peak stage were positively correlated with those in the latent phase （r =0.863-0.900, P 〈 0.01）, but negatively correlated with neurological scores at the peak stage （r=- -0.068 to -0.863, P 〈 0.05-0.01）. The IFN-γ level at the peak stage was negatively correlated to that in the latent phase （r = -0.683-0.650, P 〈 0.05）, but positively correlated to neurological scores at the peak stage （r =0.975, 0.845, P 〈 0.05）. CONCLUSION： NPY injection into the lateral cerebral ventricle can promote the secretion of IL-4, inhibit the production of IFN-γ, relieve white matter demyelination, and inhibit EAE attack in an experimental model of EAE.

Effects of WH-1 and WH-2 eye drops on experimental allergic uveitis in rabbits

Effects of WH-1 and WH-2 eye drops on experimental allergic uveitis(FAU)in rabbits induced by bovine serum albumin were clinically and pathologically observed in comparisonwith local drops of dexamethasone used as positive control.The results showed that WH-2 obvi-ously inhibited the inflammatory reactions while WH-1 did not.Protein concenwation in the aqueoushumor of WH-2-treated group of rabbits was 9.24±2.34mg/ml,which was notably lower(P【0.01)than both that of the untreated(14.33±3.14 mg/ml)and of the WH-1-treated(12.91±3.95mg/ml),but signifificantly higher than that of the dexame dexamethasone-treated goup(4.43±1.43mg/ml,P【0.01).The alleviation of the intraocular inflammatory reaction by therapy of WH-2eye drops was confimed pathologically.This study indicates that WH-2 has a positiveantiphlogistic effect on EAU in rabbits.

Effects of Qingkailing on Experimental Allergic Uveitis in Rabbits

Experimental allergic uveitis(EAU)in rabbits was induced by singleintraocular injection of bovine serum albumin(BSA).The average of protein con-centration in aqueous humor of untreated group of rabbits was 14.33±1.21mg/mland the count of tritiated thymidine(~3H-TdR)incorporated into lymphocyte T was3,987±1,156cpm/10~6.The specific antibody responses to BSA in the serum andthe aqueous were 0.508±0.034 and 0.369±0.019(OD)respectively.Meanwhile,the effect of Qingkailing on EAU was observed in comparison wi...

Effect of oxymatrine on interferon-gamma and tumor necrosis factor-alpha serum levels in an experimental rat model of autoimmune encephalomyelitis

BACKGROUND： Studies have demonstrated that experimental autoimmune encephalomyelitis （EAE） onset correlates with increased interferon-v （IFN-γ） and tumor necrosis factor-α （TNF-α） expression. Oxymatrine （OM） has been shown to inhibit autoimmune responses, but there are no reports showing that it could prevent the development of EAE. OBJECTIVE： To observe the effect of OM on serum levels of IFN-γ and TNF-α in a rat model of EAE.DESIGN, TIME AND SETTING： A randomized, controlled, animal study was performed at the Experimental Animal Center of Henan Academy of Chinese Medicine and at the Key Disciplines Laboratory Clinical Medicine of Henan Province between July and December 2008. MATERIALS： OM was purchased from Chia-tai Tianqing Pharmaceutical, China; complete Freund＇s adjuvant was purchased from Sigma, USA. METHODS： Forty female Wistar rats were randomly assigned to four groups： EAE model （M）, low-dose OM treatment （OM-L）, high-dose OM treatment （OM-H）, and normal control （N, no immunization）, with 10 rats in each group. EAE was established in the M, OM-L, and OM-H groups following immunization with Guinea pig spinal cord homogenate and complete Freund＇s adjuvant. The M and N groups were intraperitoneally injected with normal saline （6.7 mL/kg per day）, the OM-L group received an intraperitoneal injection of OM （100 mg/kg per day）, and the OM-H group received OM （150 mg/kg per day）. MAIN OUTCOME MEASURES： At 16 days after immunization, the degree of histopathological changes in the spinal cord was assessed by hematoxylin-eosin stanining. Enzyme-linked immunosorbent assay was used to detect serum levels of IFN-γ, and radioimmunoassay was utilized to determine serum TNF-α level. Neurological scores were measured on a daily basis according to a 0-5 scale. RESULTS： Daily injections of OM, both high and low doses, resulted in decreased neurological scores in EAE rats （P〈0.01）, as well as reduced cellular infiltration in the spinal cord and decreased levels of serum IFN-γ and TNF-α （P〈 0.01）. CONCLUSION： OM reduced the onset and severity of EAE, which correlated with decreased IFN-γ and TNF-α expression.

基于箍围理论内外兼治面部过敏性皮炎的临床及实验研究

目的:观察运用中医外科“箍围”理论内外兼治面部过敏性皮炎的临床观察及实验研究,对其临床疗效做出评价。方法:在治疗前、治疗第2w、4w时各记录1次,面部过敏性皮炎患者面部皮损红肿、鳞屑、瘙痒程度和皮损面积来计算疗效指数,并于第12w进行复发率的随访。实验采用尾静脉注射依文思蓝与皮下注射磷酸组胺方法制作小鼠被动皮肤过敏模型,采用皮下注射4-氨基吡啶制作小鼠瘙痒模型,对蒲菊饮进行抗敏和抗瘙痒药效学试验。结果:在改善红肿、脱屑、瘙痒、皮损面积和改善中医次症方面均有明显的疗效(P<0.05),差异均有统计学意义。治疗后2w总有效率为73.3%,治疗后4w总有效率为93.3%。蒲菊饮各给药组与对照组比较,各组均可降低小鼠的皮肤血管渗透作用,中剂量组和大剂量组均有统计学意义(P<0.01,P<0.05),说明受试样品具有减轻过敏反应的作用;但蒲菊饮口服没有止痒的效果。结论:基于箍围理论内外兼治面部过敏性皮炎,能够更好地改善面部过敏性皮炎的相关症状,值得临床推广应用。

异甘草素对实验性自身免疫性神经炎大鼠模型的影响及机制研究

目的:观察异甘草素(ISL)对大鼠实验性自身免疫性神经炎(EAN)的影响并探讨机制。方法:足底注射P257-81多肽建立EAN大鼠模型,免疫后1 h,每天腹腔注射ISL(60 mg/kg)溶液,共14 d。观测大鼠发病情况,运用HE染色及透射电镜观察坐骨神经结构,ELISA法检测血清中炎症因子水平,Western blot检测脾脏单核巨噬细胞中诱导型一氧化氮合酶(iNOS)和精氨酸酶1(Arg1)、信号转导及转录激活因子3(STAT3)包括t⁃STAT3和p⁃STAT3的蛋白表达。结果:与EAN组比较,EAN+ISL组大鼠行为评分显著降低,体重明显增加,坐骨神经中炎症细胞浸润数明显减少,坐骨神经的脱髓鞘现象明显减少,血清中白介素⁃1β(IL⁃1β)、肿瘤坏死因子⁃α(TNF⁃α)、白介素⁃6(IL⁃6)和干扰素⁃γ(IFN⁃γ)水平明显降低,脾脏单核巨噬细胞中iNOS蛋白表达显著下调,Arg1表达显著上调,p⁃STAT3蛋白表达及p⁃STAT3/t⁃STAT3比值均明显降低(P<0.05)。结论:ISL对EAN具有抑制作用,其机制可能与调控STAT3⁃巨噬细胞极化途径有关。

补气通窍方对变应性鼻炎大鼠鼻黏膜病理损伤和IgE的影响

目的:探讨补气通窍方对变应性鼻炎(AR)大鼠的治疗作用及机制。方法:将50只Wistar大鼠随机分为5组:空白组、模型组和补气通窍方低、中、高剂量组,每组10只。除空白组外,余组大鼠采用卵清蛋白(ovalbumin,OVA)与氢氧化铝[Al(OH)3]联合致敏建立AR大鼠模型。补气通窍方低、中、高剂量组分别按14.38 g/kg、28.76g/kg、57.55g/kg的剂量灌胃给予补气通窍方药液,空白组及模型组灌胃给予纯净水,各组灌胃容量均为4ml/d,连续给药7 d。给药后每天观察大鼠喷嚏、抓鼻的次数及流涕情况,末次灌胃24 h后处死各组大鼠,采用酶联免疫吸附测定法检测外周血免疫球蛋白E(IgE)的浓度,常规苏木精-伊红染色(HE染色)病理学检查鼻中隔和鼻腔外侧壁呼吸区黏膜的组织形态学变化。结果:与空白组比较,模型组大鼠行为学积分、IgE水平明显升高(P<0.01),鼻黏膜组织损伤明显。与模型组比较,补气通窍方中、高剂量组第2d~第7d的行为学评分均显著降低(P<0.05或P<0.01);补气通窍方低、中、高剂量组均能显著降低变应性鼻炎大鼠血清IgE水平(P<0.01),并能明显改善变应性鼻炎大鼠鼻组织病理损伤。结论:补气通窍方可通过降低IgE水平,减轻鼻腔黏膜炎症,延缓变应性鼻炎病情进展。

RRx-001对吉兰-巴雷综合征大鼠模型的保护作用及机制研究

目的探讨RRx-001对实验性自身免疫性神经炎(EAN)的保护作用及机制的影响。方法采用人工合成P253~78肽段与完全弗氏佐剂混合免疫Lewis大鼠建立EAN模型,RRx-001腹腔注射给药。实验分为3组:对照组、模型组和实验组。通过检测大鼠体重和临床评分,评估病情进展。采用透射电镜观察坐骨神经脱髓鞘变化。检测血液异硫氰酸荧光素―右旋糖酐,评估肠道屏障通透性。检测肠道一氧化氮(NO)、谷胱甘肽(GSH)和超氧化物歧化酶(SOD),评估氧化应激水平。采用ELISA试剂盒检测白细胞介素(IL)-1β、IL-18和肿瘤坏死因子α(TNF-α)表达情况。采用流式细胞术分析CD3^(+)T细胞、CD3^(+)CD4^(+)T细胞、CD3^(+)CD8^(+)T细胞、CD4^(+)CD44H^(+)T细胞、CD4^(+)CD62L^(+)T细胞和CD11b^(+)F4/80^(+)巨噬细胞。结果与模型组相比,RRx-001可以减少EAN大鼠体重丢失、降低临床评分(P<0.05);缓解坐骨神经脱髓鞘;提高SOD活力,降低IL-1β和TNF-α表达水平,减轻肠道损伤而改善肠通透性(P<0.001);降低CD4^(+)T/CD8^(+)T淋巴细胞和CD11b^(+)F4/80^(+)巨噬细胞比例,提升CD3^(+)T淋巴细胞的比例(P<0.05)。结论RRx-001可以改善EAN大鼠临床症状,其机制可能与调节免疫细胞活化和抑制炎症因子释放有关,发挥对EAN大鼠的保护作用。

DTI评估实验性自身免疫性神经炎兔坐骨神经损伤的可行性研究

目的探讨弥散张量成像(DTI)在兔坐骨神经实验性自身免疫性神经炎(EAN)诊断中的可行性。方法选取大耳白兔20只,实验组10只建立EAN动物模型,对照组10只。分别于0、14、18、20天行DTI扫描,进行纤维束示踪成像;并于各时间点测量并比较FA值和ADC值。结果DTI示踪成像显示EAN实验组坐骨神经较正常组边缘不光整,纤维数量减少。兔坐骨神经各时间点纤维束FA值实验组低于对照组,ADC值实验组高于对照组,差异有统计学意义。结论应用DTI活体纤维束示踪EAN动物模型坐骨神经损伤的形态变化,定量评价神经损伤是可行的。

针刺对实验性变态反应性神经炎T细胞亚群的调节作用

目的 :探讨针刺治疗变态反应性神经炎的机理。方法 :4 0只大鼠分为正常对照组、模型组、针刺组、药物组。针刺组取“L4 夹脊”“足三里”“悬钟”穴 ,药物组用泼尼松灌胃给药。用流式细胞仪检测大鼠外周血T细胞亚群的变化。结果 :模型组CD8+细胞数降低 ,CD4 +/CD8+比值明显升高。针刺组能显著提高CD8+细胞数 ,使CD4 +/CD8+比值接近正常 ,而对CD3+、CD4 +细胞数无明显影响。结论 :针刺疗法能有效调整T细胞亚群的紊乱状况。

单核细胞趋化蛋白-1和调节活化正常T细胞表达分泌因子与实验性变态反应性神经炎的关系

目的研究趋化因子单核细胞趋化蛋白-1(MCP-1)和调节活化正常T细胞表达分泌因子(RANTES)与实验性变态反应性神经炎(EAN)发病的关系,探讨EAN的免疫发病机制.方法给Wistar大鼠足垫皮下注射兔坐骨神经匀浆建立EAN模型,用免疫组化技术检测EAN大鼠发病不同时间坐骨神经MCP-1和RANTES的表达.结果EAN组的MCP-1表达第9 d达高峰,随后逐渐下降,第15 d、21 d、28 dMCP-1的表达与前一时间点比较差异均有显著性(均P＜0.01);第9 d、15 d、21 d MCP-1表达均显著高于对照组(均P＜0.001).EAN组第9 d、15 d、21d RANTES表达均显著高于对照组(P＜0.01～0.001),第15 d表达最高.结论MCP-1和RANTES在EAN的发病过程中发挥了重要作用,MCP-1可能起始动作用,RANTES可能与EAN的病情进展有关.

针刺对实验性变态反应性神经炎TNF-α和IL-4的影响

目的 探讨肿瘤坏死因子 - α(TNF- α)和白细胞介素 - 4 (IL- 4 )与实验性变态反应性神经炎 (EAN)发病的关系 ,从细胞因子水平研究针刺疗法对本病的免疫调节作用。方法 4 0只大鼠分为正常对照组、模型组、针刺组、药物组 ,建立大鼠 EAN动物模型 ,观察大鼠发病率及致病程度 ,针刺组取腰 4 夹脊、足三里、悬钟穴 ,药物组用泼尼松灌胃给药。采用双抗体夹心 EL ISA法 ,检测大鼠血清的 TNF- α和 IL- 4的含量变化。结果 模型组 TNF- α含量较正常组明显升高。针刺组和药物组均能降低TNF- α的含量 ,使其水平接近正常 ,尤以药物组抑制作用明显。IL- 4的含量各组间均无明显差异。结论 提示本病存在 Th1/Th2细胞因子间的失衡 ,其中以 Th1型细胞占优势。针刺主要是通过抑制 TNF- α等 Th1细胞 ,来重建细胞因子间的平衡。

过敏煎对SD大鼠血中IgE变化影响的实验研究

目的:通过测定哮喘大鼠血中IgE的变化,观察过敏煎对哮喘大鼠免疫功能的影响并分析其作用机制。方法:用抗原液致敏SD大鼠,以抗原攻击后建立哮喘模型,采用酶联免疫吸附试验(ELISA)测定血清中免疫球蛋白E(IgE)水平。结果:过敏煎对过敏性哮喘有显著的治疗作用(P<0.05)。结论:过敏煎可以对抗IgE介导的Ⅰ型变态反应,表明过敏煎具有治疗哮喘的作用。