阻断5-HT1B受体对正常和帕金森病大鼠底丘脑核神经元活动的不同作用

目的观察体循环给予5-HT1B受体拮抗剂SB224289后,对正常大鼠和帕金森病(Parkinsons disease,PD)模型大鼠底丘脑核(subthalamic nucleus,STN)神经元电活动的影响。方法采用在体细胞外记录的方法,研究正常和PD大鼠STN神经元电活动的变化;比较阻断5-HT1B受体后两组大鼠STN神经元电活动的改变。结果①PD组大鼠STN神经元的平均放电频率[(7.87±1.37)Hz]明显高于正常组大鼠[(6.59±1.44)Hz,P<0.001]。两组大鼠STN神经元均表现为规则、不规则和暴发式放电3种形式。正常组大鼠具有规则、不规则和暴发式放电的神经元比例分别为33.33%、54.17%和12.50%;PD组分别为31.25%、35.42%和33.33%,PD组大鼠具有暴发式放电的神经元的百分比显著高于正常组(P<0.01)。②阻断5-HT1B受体后,正常大鼠STN神经元平均放电频率明显增高(P<0.01),具有暴发式放电的神经元数量显著增多(P<0.05)。而PD组大鼠阻断5-HT1B受体后STN神经元的放电频率和放电形式均无明显变化。结论 PD大鼠STN神经元呈过度兴奋状态;阻断5-HT1B受体可兴奋正常大鼠的STN神经元,而不影响PD大鼠的神经元活动。     

正常人及肠易激综合征患者肠黏膜孤啡肽受体的表达

目的检测正常人及肠易激综合征(IBS)患者肠黏膜孤啡肽受体(ORL-1)的表达,探讨其在IBS患者发病机制中的作用。方法黏膜标本取自20例正常人和27例腹泻型(D-IBS)、23例便秘型(C-IBS)患者空肠上段及升结肠,应用实时荧光定量RT-PCR法对肠黏膜ORL-1的表达进行定量分析。结果正常对照组空肠上段及升结肠均有ORL-1mRNA的表达,且空肠上段表达量高于升结肠(P<0.05);D-IBS患者空肠及升结肠黏膜ORL-1mRNA表达量均低于正常对照组(P<0.05),C-IBS患者与正常对照组间无差异。结论 ORL-1受体在人胃肠运动及IBS的病理生理机制中可能具有重要作用;OFQ/ORL-1系统对IBS不同亚型的调节具有异质性。     

溃疡性结肠炎大鼠血清酪酪肽水平及其受体特性的测定

目的 通过测定溃疡性结肠炎(UC)大鼠血清酪酪肽(PYY)水平及其空肠黏膜上皮细胞膜PYY受体的特性来观察UC时血清PYY水平及其受体的变化.方法 将大鼠随机分成UC组、腹泻型肠易激综合征(D-IBS)组及对照组,用同位素放射免疫法分别检测各组的PYY水平及反映受体特性的两个参数:平衡解离常数(Kd)和最大结合容量值(Bmax).结果 UC及D-IBS组血清PYY水平高于对照组(P<0.001),且UC组亦高于D-IBS组(P<0.001);但UC组Kd及Bmax值与正常组和D-IBS组比较均无明显差异(P>0.05).结论 UC组PYY水平高于正常及D-IBS组,推测UC时PYY水平的变化可能与其腹泻症状和炎症病变的产生有关;UC组的Kd及Bmax与正常组比较无显著变化,推测UC可能与PYY受体的变化无关.     

Induction of animal model of Graves' disease in BALB/c mice

Objective To construct an animal model of Graves' disease (GD) by immunizing BALB/c mice with hM12 cells co-expressing major histocompatibility complex (MHC) class Ⅱ molecules and human thyrotropin receptor (TSHR) molecules. Methods BALB/c mice in experimental group (H-2d) were immunized with hM12 cells Intraper-itoncally every 2 weeks for six times, while mice in control group were immunized with M12 cells. Five weeks later, the thyroids were histologically examined, and serum samples were tested for thyroid-stimulating antibodies (TSAb) and thyroid hormone levels. Results One BALB/c mouse in experimental group developed Graves'-like disease. Total T4 and T3 levels in this mouse were above the upper limit of normal, TSAb activity was displayed in its serum. The thyroid histologically showed the features of thyroid hyperactivity including thyrocyte hypercellularity and colloid absorption.None of control mice developed Graves'-like disease. Conclusion An animal model with some characteristics of human Graves' disease was successfully induced and the model will facilitate studies aimed directly at understanding the patho-genesis of autoimmunity in Graves' disease.     

Glutamate enhances the expression of vascular endothelial growth factor in cultured SD rat astrocytes

Objective To study the effect of glutamate on the expression of vascular endothelial growth factor (VEGF) mRNA and protein in cultured rat astrocytes. Methods Cultured rat astrocytes were randomly divided into 6 groups: control group (C), glutamate group (G), QA group (Q), DCG-IV group (D), L-AP4 group (L) and glutanmte-FMCPG gronp (G+M). Cells were cultured under nomoxic condition (95% air, 5% CO2). RT-PCR and ELISA methods were used to detect the expression of VEGF mRNA and protein in cultured astrocytes, respectively. G+ M group was preincubated with lmM MCPG for 30 min prior to the stimulation with glutamate. There were 7 time points at 0,4,8,12,16,24 and 48 h in each group except G+M group. Results The expression of VEGF mRNA and protein did not differ significantly among D group, L group and C group. Different from that in C group, the expression of VEGF mRNA and protein could be enhanced both in a dose-dependent and time-dependent manner in G group and Q group. Meanwhile, the enhanced expression of VEGF mRNA and protein in G group was completely suppressed by MCPG after 24 h. Conclusion Glutamate can increase the expression of VEGF mRNA and protein in cultured astrocytes, which may be due to the activation of group I metabotropic glutamate receptors in astrocytes.     

用流式细胞测定仪测定AITD患者TRAb

以人工重组ＴＳＨ受体表达的中国仓鼠卵细胞（ＣＨＯ－ＴＳＨＲ）为靶细胞,用流式细胞（ＦＡＣＳ）测定技术,对４５例自身免疫性甲状腺病（ＡＩＴＤ）患者血清中ＳＨ受体抗体（ＴＲＡｂ）进行测定。结果显示：３６例ＧＤ患者阳性细胞结合的百分数为１．９％～７７．４％。阳性率为９１．６６％。其均值２６．１３９％与正常人均值６．１６３％相比有显著性差异（Ｐ＝０．０００１）。９例桥本（ＨＴ）甲减患者５例阳性,阳性率为５５．５６％。证实以ＣＨＯ－ＴＳＨＲ细胞为靶细胞用ＦＡＣＳ进行ＴＲＡｂ汕测定不失为一种敏感简便的新方法。     

肺癌性激素及其受体之间关系的研究

为研究肺癌的发病机制，探讨其性激素及其受体之间的关系，运用酶联亲合组化法对53例肺癌癌组织中雌激素受体（ER）和孕激素受体（PR）进行了检测，同时采用R抗体放射免疫分析法测定了患者外周血中的雌二醇（SEL）和孕酮水平（SPL）。结果显示ER阳性率49．1％，PR阳性率54．7％。SEL、SPL均有明显的升高（P<0．05），无论ER（＋）组还是ER（－）组，SEL均有显著的升高（P＜0．05）；ER（＋）组、PR（＋）组、ER（＋）和PR（＋）组的SEL、SPL较ER（－）组、PR（－）组、ER（－）和PR（－）组的相对低。提示受体阳性者更多地受到性激素的影响。     

FUCOIDIN INHIBITS OXIDIZED LOW DENSITY LIPOPROTEIN FROM INDUCING HUMAN PERIPHERAL BLOOD MONOCYTE EXPRESSION OF PROINFLAMMATORY CYTOKINES mRNA

Researcheshavealreadydemonstratedthatscav engerreceptorclassA(SR A)isabletobindoxidizedlowdensitylipoprotein(OxLDL)withhighaffinityandisoneofthemainreceptormediatingmurinemacrophagetouptakeOxLDL[1] .Itisalsoexpressedinhumanperipheralbloodmonocyte[2 ] andathero scleroticlesions[3 ] .However ,functionsofSR Ainmediatinghumanperipheralbloodmonocytetoup takeOxLDLaswellaspromotingtheatheroscleroticimmuno pathologicallesioninthelocalbloodvesselarestillunclear .Soforthepurposeofstudyingthefunc…     

选择性PDGF受体酪氨酸激酶抑制剂对兔PVR的治疗作用

目的　评价一种新的血小板源性生长因子 (platelet derivedgrowthfactor,PDGF)受体酪氨酸激酶抑制剂AG12 95对兔增殖性玻璃体视网膜病变 (proliferativevitreoretinopathy ,PVR)的治疗作用。 方法　兔结膜成纤维细胞 (rabbitconjunctivalfibroblastscells,RCF)培养 ,用MTT分析法检测PDGF AA和 BB以及AG12 95对兔RCF的增殖状况的影响。建立PVR动物模型 ,玻璃体腔内给予AG12 95 ,用牵引性视网膜脱离 (tractionalretinaldetach ment,TRD)的发生率判断药物的体内疗效。眼视网膜电生理检查和HE染色分析药物的毒性。结果　 10 μmol·L-1和 10 0 μmol·L-1两种浓度的AG12 95均可显著抑制由PDGF AA和 BB诱导的成纤维细胞的增生 ,10 0 μmol·L-1AG12 95可减缓兔TRD的发生 ,但其作用仅持续至第 2 1d。在AG12 95治疗组中 ,未发现明显的网膜毒性。结论　PDGF受体酪氨酸激酶抑制剂AG12 95可减缓兔TRD的发生。     

结肠癌血管的肾上腺素受体和内皮素受体

目的研究结肠癌患者癌动脉的收缩功能。方法取结肠癌癌患部位动脉、癌旁10 cm处动脉、非癌患者动脉,用动脉张力描记法记录血管活性物质收缩血管的量效曲线。结果去甲肾上腺素(NA)引起正常人结肠动脉的最大收缩(Emax)和最大收缩浓度的负对数(pD2)分别为(97±19)%和5.94±0.17;结肠癌动脉NA收缩的Emax和pD2明显低于癌旁动脉(P<0.01)和正常人结肠动脉(P<0.05)。ETB受体激动剂S6c在结肠动脉不引起收缩。ET-1对正常人结肠动脉收缩的Emax和pD2分别为(106±7)%和8.85±0.17;ET-1引起结肠癌动脉的Emax明显低于癌旁动脉(P<0.01);引起结肠癌动脉的pD2与癌旁动脉无明显差异(P>0.05)。结论α受体和ETA受体是结肠癌动脉的主要缩血管受体。