药物缓释载体材料在医药领域中的研究及应用

背景：药物缓释就是将小分子药物与高分子载体以物理或化学方法结合,在体内通过扩散、渗透等控制方式,将小分子药物以适当的浓度持续地释放出来,从而达到充分发挥药物功效的目的。 目的：总结药物缓释载体材料特征及其在医药领域中的应用。 方法：以“药物缓释、载体材料、生物降解、壳聚糖、聚乳酸、海藻酸钠”为中文关键词,以“Drug delivery,carrier material,biodegradable,chitosan,polylactic acid, sodium alginate”为英文关键词,采用计算机检索中国期刊全文数据库、PubMed数据库(1993-01/2010-11)相关文章。纳入高分子生物材料-药物缓释载体等相关的文章,排除重复研究或Meta分析类文章,共入选31篇文章进入结果分析。 结果与结论：壳聚糖和聚乳酸是当前在药物缓释体系中应用较多的材料,它是将小分子药物与高分子载体以物理或化学方法结合, 以适当的浓度持续地释放出来,从而达到充分发挥药物功效的目的,较单一生物材料具有显著优越性,具有更好的生物相容性和生物可降解性。目前很多研究仍处于实验阶段,还有一些问题有待于解决,如制剂质量方法不成熟,剂量较难控制,成本较高等。     

药物缓释载体材料类型及其临床应用

摘要目的：文章对目前国内外几种重要载体材料的临床应用情况进行了阐述。方法：作者以“药物载体,缓释材料,生物降解”为检索词,在中国期刊全文数据通据库(CNKI：1989/2010),采用电子检索的方式对所有相关文献进行了详细检索。排除Meta分析及重复性研究,最终入选20篇文献进入结果分析。结果：生物降解性合成高分子材料安全、可靠,有良好的生物相容性,成为药物缓释载体的首选材料;壳聚糖作为药物缓释载体在减少给药次数,降低药物毒副作用,提高药物疗效等方面具有重要作用;纳米纤维载体可明显增强药物缓释效果;纤维蛋白生物相容性好, 是良好的药物缓释载体。结论：药物控制释放体系在机体内可以显示出被动靶向以及缓释等多种优点,它是药物缓释体系的重要组成部分,也是影响药效的主要因素。关键词：药物载体;缓释材料;生物降解;壳聚糖;纳米纤维;纤维蛋白doi:10.3969/j.issn.1673-8225.2010.47.031     

缓释药物的研究进展及临床应用

背景：各种制备缓释制剂的缓释材料很多,目前可用于生产的缓释材料有40多种,广泛应用于临床多种疾病的治疗。目的：对目前国内外几种重要的缓释药物载体材料及临床上常用的缓释药物进行总结。方法：应用计算机检索CNKI和PubMed数据库2000-01/2010-12关于缓释药物研究的文章,在标题和摘要中以“缓释,药物,生物材料”或“sustained release,drug,biomaterials”为检索词进行检索。选择文章内容与缓释药物密切相关的文章。排除Meta分析及重复性研究,最终纳入23篇文献进入结果分析。结果与结论：可生物降解的合成高分子材料受到普遍重视并得到广泛应用,壳聚糖以其良好的性能备受青睐,成为药物缓释的一种重要载体,生物降解高分子聚乳酸在药物缓释方面的应用,起到重要的治疗作用;纤维蛋白胶生物相容性高,能有效延缓药物释放,在临床很多领域广泛应用。     

药物控释载体材料的性质

学术背景：将药物或其他的活性物质与适当的载体按一定的形式制成的药物控释制剂已成为药学领域的重要发展方向，然而不同性质的药物载体材料具有不同的药物释放行为，为了获得令人满意的释药速率，新型药物载体材料的研究成为近年来的研究重点。 目的：介绍几种用作药物载体的材料，分析材料的性质及其在药物控释中的应用。 检索策略：由该论文作者应用计算机检索中国期刊全文数据库1998-01/2007-06的相关文献，检索词：“高分子水凝胶，聚乳酸，壳聚糖，丝素蛋白，药物控释，药物载体”，限定文章语言种类为中文。纳入标准：①不同类型药物载体材料的制备及性能；②不同类型药物载体材料的药物控释性研究。排除标准：较陈旧的文献。 文献评价：共检索到86篇相关文章， 28篇符合标准，其中10篇为综述，其余为临床或基础实验研究。 资料综合：①目前用作药物载体的材料主要包括高分子凝胶、聚乳酸（PLA）/乳酸-羟基乙酸（PLGA）、壳聚糖及其衍生物、丝素蛋白等。②智能高分子水凝胶对温度、酸度、压力、光等引起的刺激，能及时地作出溶胀和收缩应答的智能效应，这种特殊的环境敏感性使它被广泛地应用于药物缓释体系。③聚乳酸和聚乳酸-羟基乙酸是一种生物可降解高分子材料，具有生物相容性、生物可降解性、降解产物无毒等优点，用作药物控释载体材料时,可通过调节聚乳酸的降解速率改变释放速率，提高药效。④壳聚糖具有很好的吸附性、成膜性和通透性，较低相对分子质量的水溶性壳聚糖更易在体内降解，不易积聚， 以壳聚糖为载体材料制备纳米粒、微球等给药系统是近年来的研究热点。⑤天然高分子材料丝素蛋白无毒、无刺激,具有良好的物理、化学、生物学性能,与人体有较好的组织相容性，在负载与释放药物时, 具有一定程度的pH 值响应性和酶分解性。一般通过化学修饰、添加其他化合物等方法, 提高丝素蛋白的性质，增加丝素蛋白质对药物的吸附释放功能。 结论：不同类型药物载体材料均具有很好的生物相容性、生物可降解性、理化及生物稳定性和极低的毒性，且有较高的载药性，但在实际应用过程中还需要对材料的性能进行合成和改进，使其具有特定性能、结构，满足不同药物制剂释放的要求。     

胶原蛋白复合壳聚糖支架的制备及生物学性状：壳聚糖及胶原比例筛选

背景：壳聚糖和胶原类支架已成为组织工程常用的载体材料。但是,现阶段如何能够通过调节二者比例而达到理想的细胞载体仍是目前需要解决的问题之一。 目的：调节胶原与壳聚糖二者配制比例制备支架材料,检测及对比不同比例支架材料生物学性质。 方法：制备1∶1,1∶2,1∶3,1∶4,1∶5比例的壳聚糖、Ⅰ型胶原蛋白成分,经紫外线交联后冷冻干燥,再将其用NAOH与蒸馏水进行中和,二次冻干制备好支架。观察不同比例支架的材料性质、孔隙率、降解率、溶胀率;扫描电镜观察孔径的大小及形态。 结果与结论：在壳聚糖含量固定,支架的大体孔径经统计比较差异有显著性意义(P < 0.05)。1∶3比例制备的孔径最大,达到(298.0±36.0) μm;支架总体的孔隙率为93.9%~97.5%,胶原比例的增加对支架孔隙率的影响较轻微。各组支架的溶胀率可达到80%左右,支架的溶胀程度随胶原比例增加而减少。在支架的降解率随着胶原比例增加而增加,而壳聚糖含量越高,降解速度越慢。结果证实,通过紫外光交联法,按照1∶3 配比的胶原和壳聚糖的支架材料更加适合软骨组织工程的要求。 关键词：壳聚糖;胶原蛋白;支架;紫外线交联;组织工程 doi:10.3969/j.issn.1673-8225.2010.29.012     

壳聚糖季铵盐的最新研究进展*★

学术背景：壳聚糖作为一种性能卓越的生物材料已广泛应用在各个领域，但其在某些方面还存在一定的缺陷和不足。对壳聚糖进行改性可以得到新的衍生物壳聚糖季铵盐，增强了正电性和在水中的溶解性，体现壳聚糖季铵盐在生物医学方面的新性能。 目的：综述壳聚糖季铵盐在生物医学和轻工业等领域的最新研究进展。 检索策略：查找有关壳聚糖季铵盐应用研究方面的文献，应用计算机检索PUBMED数据库和EBSCO数据库，检索词“quaternary AND chitosan”，年限不限，限定语言为英语；计算机检索维普资讯中文科技期刊数据库，检索词为“壳聚糖，季铵盐”，年限为1989/2007，限定语言为中文。同时手工检索有关书籍。在PUBMED上共收集到39篇相关的英文文献，在EBSCO数据库中搜索到55篇相关的英文文献，在维普资讯上共搜索到55篇相关的中文文献，对文献进行筛选，并确定纳入标准：①选取针对性强，相关度高的文献。②对同一领域的文献选择近期发表或权威杂志的文献；排除重复研究和Meta分析类文章。最后27篇被选用。 文献评价：选用27篇文献，均为临床与实验研究。 资料综合: 壳聚糖作为优良的生物材料，应用已十分广泛，但是它的水不溶性限制了它在很多方面的运用。新的壳聚糖衍生物壳聚糖季铵盐克服了壳聚糖本身的溶解性差的缺点，在生理条件下也能很好地溶解，在生物相容性、抗菌性、吸湿保湿等性能方面均明显优于壳聚糖。 结论：壳聚糖季铵盐的研究已经成为各领域研究的新热点，其应用前景将更加广阔，对相关作用的认识有待于进一步深入。     

载表皮生长因子/壳聚糖纳米粒纤维蛋白胶胶联羊膜的制备及体外释药评价

背景：纤维蛋白胶胶联羊膜作为一种无需缝合生物移植材料还无法有效地在局部长时间缓释药物,特别是对于一些不稳定的生物活性蛋白药物。 目的：构建新型的能有效缓释蛋白药物的载表皮生长因子壳聚糖纳米粒纤维蛋白胶羊膜复合体。 方法：制备表皮生长因子/壳聚糖载药纳米粒并考察其表征,然后将载药纳米粒掺入纤维蛋白胶,再将载纳米粒的纤维蛋白胶和羊膜胶联黏合,制备出负载表皮生长因子/壳聚糖纳米粒纤维蛋白胶胶联羊膜,并进行形态学和体外释药观察,检测释放出的表皮生长因子生物活性。 结果与结论：表皮生长因子/壳聚糖纳米粒的粒径为(275.7±6.8) nm,Zeta电位为(32.7±0.6) mV,包封率为(67.03±1.22)%,多分散指数为0.23±0.04,形态圆形均一,载纳米粒纤维蛋白胶能够很好地与羊膜胶联黏合,表面呈网状结构,纳米粒充斥其中。载表皮生长因子/壳聚糖纳米粒纤维蛋白胶胶联羊膜体外释药可达14 d,释放的表皮生长因子生物活性可保持7 d以上。说明制备的载重组人表皮生长因子/壳聚糖纳米粒纤维蛋白胶胶联羊膜作为一种无缝合生物移植材料可在局部缓慢释放表皮生长因子。     

药物洗脱支架的药物装载方式及应用

摘要 背景：药物释放动力学不理想、高分子载体引起的后期血栓和涂层完整性破坏等是目前药物洗脱支架面临的主要问题。要从根本上解决这些问题,就需要改变支架上药物的装载方式,包括药物和载体的选择以及药物涂层的制备工艺。 目的：讨论目前药物洗脱支架的药物装载方式,探索其可能的发展方向。 方法：应用计算机检索 Elsevier、ACS和Springerlink数据库中 2000-03/2010-01关于药物洗脱支架涂层的文章,在标题中以 “stent; drug; coating ”为检索词进行检索。选择文章内容与药物洗脱支架涂层有关者,同一领域文献则选择发表在权威杂志的文章。初检得到445篇文献,根据纳入标准选择关于药物洗脱支架涂层制备的31篇文章进行综述。 结果与结论：目前研究的药物洗脱支架涂层按照药物与其载体间的结合方式可分为物理装载,静电吸附和化学键合。文章分别讨论了不同体系的药物、载体、涂层制备、释放动力学和降低再狭窄效果,指出不同的药物根据其自身的生物、物理和化学性质,可以选择合适的载体和改变涂层制备工艺,从而达到相对理想的释放动力学。另外还展望了药物洗脱支架涂层的未来发展方向,有望为该领域提供新的思路和方法。 关键词：药物洗脱支架;涂层制备;药物装载;药物载体;释放动力学;支架再狭窄 doi:10.3969/j.issn.1673-8225.2010.42.021     

壳聚糖载氟喹诺酮类药物缓释微球的制备及应用*

壳聚糖载氟喹诺酮类药物微球有多种制备方法,如沉淀析出法、乳化交联法、喷雾干燥法和离子凝胶法等。不同的制备方法具有各自的优点和不足,但其释药机制基本相同。这类药物微球具有增强氟喹诺酮类药物抗耐药菌的能力,主要用于局部及全身组织的消炎与抗感染。文章以近几年国内外论文为依据,进行分析,归纳和总结。介绍了壳聚糖载氟喹诺酮类药物缓释微球的制备方法和释药机制,探讨了缓释微球作用特点及应用状况。壳聚糖载氟喹诺酮类药物微球具有良好的缓释、抗菌性能,对其进行纳米化,开发纳米粒新剂型,具有重要的科研和应用价值。     

70002vip/纳米药物的靶向作用及不良反应

纳米技术(nanotechnology)是指用单个原子、分子制造或将大分子物质加工成粒径为1—100 nm物质的技术。纳米技术已在药物制剂领域被广泛深入地研究和应用,通过纳米技术制成载药纳米微粒和纳米药物制剂。纳米药物与普通制剂的药物相比,具有较大的表面积、较强的化学活性、较快的吸收速度,在通过生物体的各种屏障、控制药物的释放速度、设定药物的靶向性等许多方面,纳米药物都具有一般药物不可替代的优越性,药物纳米制剂的靶向性纳米药物制剂与以往药物剂型比较,最突出的优点是具有明显的靶向性。也就是说它能将药按设计途径输送到药物的靶位。当前大多数纳米药物制剂的靶向性研究都选择肿瘤细胞为靶位。研究的目标是：将药物送到特异的组织、器官,甚至单个细胞、细胞器区域浓集或释药,使药物在靶位保持有效浓度和足够的时间,而摄取到全身的剂量很少。这样不仅可提高疗效,而且可降低药物的不良反应。纳米药物作为崭新的一类制剂,为治疗一些难治性疾病提供了一个崭新的思路,给医药界带来了观念性变革,受到医药界的广泛关注。     

Presynaptic modification of neuromuscular transmission by antiacetylcholine receptor antibody: myasthenic serum and monoclonal antibody produced by transformed lymphocytes

When myasthenic serum or a monoclonal antiacetylcholine receptor (anti-AChR) antibody produced by human transformed lymphocytes and transferable to an animal was applied to rat diaphragms in vitro, presynaptic facilitation was demonstrated by changes in ACh quantal content of endplate potentials. The results correlated with ability of the antibody to block binding of alpha-bungarotoxin to AChR, but not with titers of anti-AChR antibody by immunoprecipitation assay and AChR degradation rate. Antibody to the receptor site near the ACh-binding site may act presynaptically to compensate for the postsynaptic failure in myasthenia gravis.     

Uric acid levels and dopamine transmission in rat striatum: diurnal changes and effects of drugs

Carbon paste disc electrodes were used to detect voltammetrically changes in the extracellular concentration of the purine metabolite, uric acid, and the dopamine metabolite, homovanillic acid (HVA), in the striatum of unanaesthetized, unrestrained rats under a variety of conditions. The motor activity level for each rat was recorded between the electrochemical scans. In totally unperturbed animals, there was a significant correlation between the levels of the two metabolites during the bright, relatively inactive, period of the diurnal cycle. During much of the dark (active) phase of the cycle, however, the uric acid signal showed no significant change compared with the light-on period, in contrast to the HVA signal which showed a marked increase. Significant variations in the concentration of striatal uric acid were observed during the switch-over from light to dark and dark to light conditions. The unilateral infusion of gamma-aminobutyric acid, taurine and haloperidol into the substantia nigra caused increases in the height of both the uric acid and HVA peak in the ipsilateral striatum; the size of these changes showed a significant correlation. Variable changes occurred on the contralateral side where no correlation was observed. Intraperitoneal administration of the mixed dopamine-receptor agonist, apomorphine, and the mixed antagonist, haloperidol, did not affect striatal uric acid levels significantly. These results suggest that, although there are conditions where parallel changes in dopamine release/receptor-activation and uric acid levels do occur in the striatum, neither the release of dopamine nor activation of dopamine receptors need necessarily lead to changes in the extracellular concentration of uric acid.     

Differential ability of tissue factor antibody clones on detection of tissue factor in blood cells and microparticles

Introduction

Tissue factor (TF), the primary initiator of coagulation in vivo, plays a major role in both thrombosis and hemostasis. The expression of TF in monocytes is well documented, but its presence in other blood cells has been disputed, possibly due to methodological variations among different studies.

Materials and methods

We studied TF expression on platelets, monocytes, lymphocytes and microparticles (MPs) by flow cytometry (FCM) with five commercially available mouse anti-human TF antibodies (HTF-1, TF9-10H10, CLB/TF-5, VIC7 and VD8). The ability of different TF antibodies to inhibit cell surface TF activity was explored by incubating LPS-stimulated monocytes and MPs derived from LPS-stimulated monocytes (MMPs) with TF antibodies followed by measuring TF activity.

Results

HTF-1 detected TF only on LPS-stimulated monocytes, whereas, TF9-10H10 and VD8 detected TF associated with MPs and MMPs in addition to LPS stimulated monocytes. Surprisingly, CLB/TF-5 and VIC7 detected TF on platelets, monocytes even under unstimulated conditions, in addition to MPs and MMPs. CLB/TF-5 also detected TF on unstimulated lymphocytes. Inhibitory studies showed that at a final concentration of 10 μg/mL, HTF-1, CLB/TF-5 and VD8 inhibited monocyte TF activity by 81-84% and MMP TF activity by 92-96%; whereas TF9-10H10 had no inhibitory effect on TF activity in monocytes and MMPs.

Conclusions

Our results suggest non-specific binding by the CLB/TF-5 and VIC7 antibodies in a FCM test system and explain at least some of the reports on TF presence in blood cells, particularly TF associated with platelets and MPs. TF9-10H10 and VD8 are more suitable to detect TF on MPs by FCM.     

生物材料研究经典论文、核心著者与期刊：SCI收录生物材料类期刊的引文分析

摘要 背景：第九次世界生物材料大会将于2012年在中国召开,中国生物材料科学研究已开始同国际接轨,其相关研究也成为热点,其发表的论文数量、作者人群和期刊品种非常之多,研究者很难从众多的文献中寻找资料。 目的：为使国内研究者了解国际相关研究轨迹和前沿,文章从引文分析的角度,选取SCI生物材料领域的10种期刊发文的引文进行分析,以获取该领域研究者所需的经典论文、核心著者和核心期刊,以期对相关研究者有帮助。 方法：应用计算机检索SCI(科学引文数据库)收录生物材料期刊,并根据其影响因子选取期刊,下载到所刊登文章引文 406 753条,并对数据利用Excl和Access进行统计分析。 结果与结论：经过统计分析获取Tissue engineering等10篇经典论文、Hench, Larry L.等10位核心作者和Biomaterials等20种核心期刊,生物材料相关科技者着重研究所列经典文章,掌握相关核心作者的研究动态,着重阅读上述核心期刊可以对相关研究有帮助。 关键词：引文分析;生物材料;经典论文;核心著者;核心期刊 doi:10.3969/j.issn.1673-8225.2011.12.027     

Neurocan基因蛋白表达及其抗体制备与检测的实验研究

目的 制备Neurocan蛋白,用此蛋白免疫动物制备抗血清,并对抗血清进行检测,最终使待参与DNA疫苗构成的Neurocan蛋白所产生的抗体能与脑内创伤Ⅸ的相应抑制性蛋白抗原结合,从而减轻抑制因子对神经生长的抑制作用,促进神经再生. 方法 合成]Weuroc011,基因,构建原核表达质粒PET30a-Neurocan,转化大肠杆菌BL21.异丙基-β-D.硫代半乳糖苷(IPTG)诱导表达目的 蛋白,并经SDS-PAGE、Western blot鉴定.Neurocan蛋白免疫兔制备免疫血清.ELISA法检测抗血清效价,以兔免疫前血清为阴性对照;Western blot检测抗血清特异性,以免疫血清为一抗,山羊抗兔-AP为二抗,NBT/BCIP显色. 结果 合成的Neurocan基因经酶切鉴定、PCR鉴定及测序鉴定,显示序列正确.原核表达Neurocan蛋白经过SDS-PAGE鉴定,条带大小约为55 000,与计算出来的大小一致;经Western blot鉴定.目的 蛋白能与his抗体特异性结合,说明是Neurocan,基因的表达产物.抗血清经ELISA法检测.抗血清效价达到1:100万;经Western blot检测.目的 条带明显. 结论 Neurocan蛋白原核表达成功;通过Neurocan蛋白免疫兔可得到特异性抗体,此抗体能与Neurocan蛋白特异性结合,为DNA疫苗的进一步研制奠定了基础.     

GFA protein reactivity in nerve sheath tumors: a polyvalent and monoclonal antibody study

We studied glial fibrillary acidic (GFA) protein immunoreactivity in 30 schwannomas, including two intracerebral examples, 26 neurofibromas and 12 neuromas using the immunoperoxidase method with a polyvalent antiserum (PVAS) and three well-characterized monoclonal antibody (MAb) preparations. Twelve of the schwannomas, including both intracerebral tumors, two of the neurofibromas and none of the neuromas immunostained with PVAS. Except for one schwannoma, all the PVAS-positive tumors were positive with two of the MAb preparations. While both of the intracerebral schwannomas were positive with the third MAb, none of the extracerebral tumors were. Our results suggest that: 1) human nerve sheath tumors contain cells having polypeptides that share epitopes with GFA protein, but 2) these polypeptides differ from astrocytic GFA protein by at least one epitope, and 3) the location of the tumors in relation to the central nervous system may influence GFA protein immunoreactivity.     

Protein S and factor V in regulation of coagulation on platelet microparticles by activated protein C

Introduction

Platelets are the main source of microparticles in plasma and the concentration of microparticles is increased in many diseases. As microparticles expose negatively charged phospholipids, they can bind and assemble the procoagulant enzyme-cofactor complexes. Our aim was to elucidate possible regulation of these complexes on microparticles by the anticoagulant protein C system.

Materials and methods

Platelets were activated with thrombin ± collagen or the calcium ionophore A23187 ± thrombin to generate microparticles. The microparticles were analyzed using flow cytometry and functional coagulation assays to characterize parameters with importance for the activated protein C system.

Results

Activation with A23187 + thrombin was most efficient, fully converting the platelets to microparticle-like vesicles, characterized by high lactadherin and protein S binding capacity. Suppression of thrombin generation by activated protein C in plasma spiked with these microparticles was dependent on the presence of plasma protein S. Experiments with purified components showed that activated protein C inhibited both factor Va and factor VIIIa on the microparticle surface. Inhibition of factor Va was stimulated by, but not fully dependent on, the presence of protein S. In the factor VIIIa-degradation, activated protein C was dependent on the addition of protein S, and exogenous factor V further increased the efficiency.

Conclusions

Protein S is crucial for activated protein C-mediated inhibition of thrombin generation on platelet-derived microparticles in plasma. Moreover, protein S and factor V are synergistic cofactors in the inhibition of factor VIIIa. The results demonstrate that the activated protein C system has the capacity to counterbalance the procoagulant ability of microparticles.     

Neurophysiological and immunohistochemical studies of IgG anti-GM1 monoclonal antibody on neuromuscular transmission: effects in rat neuromuscular junctions

Guillain–Barré syndrome, which is a variant of acute inflammatory neuropathy, is associated with anti-GM1 antibodies and causes ataxia. We investigated the effects of IgG anti-GM1 monoclonal antibody (IgG anti-GM1 mAb) on spontaneous muscle action potentials in a rat spinal cord–muscle co-culture system and the localization of IgG anti-GM1 mAb binding in the rat hemi-diaphragm. The frequency of spontaneous muscle action potentials in innervated muscle cells was acutely inhibited by IgG anti-GM1 mAb. When cultures were pretreated with GM2 synthase antisense oligodeoxynucleotide, IgG anti-GM1 mAb failed to inhibit spontaneous muscle action potentials, demonstrating the importance of the GM1 epitope in the action of IgG anti-GM1 mAb. Immunohistochemistry of rat hemi-diaphragm showed that IgG anti-GM1 mAb binding overlapped with neurofilament 200 (NF200) antibodies staining, but not α-bungarotoxin (α-BuTx) staining, demonstrating that IgG anti-GM1 mAb was localized at the presynaptic nerve terminal. IgG anti-GM1 mAb binding overlapped with syntaxin antibody and S-100 antibody in the nerve terminal. After collagenase treatment, IgG anti-GM1 mAb and NF200 antibodies did not show staining, but α-BuTx selectively stained the hemi-diaphragm. IgG anti-GM1 mAb binds to the presynaptic nerve terminal of neuromuscular junctions. Therefore, we suggest that the inhibitory effect of IgG anti-GM1 mAb on spontaneous muscle action potentials is related to the GM1 epitope in presynaptic motor nerve terminals at the NMJs.     

Anti-MAG antibody and antibody complexes: detection by radioimmunoassay

A radioimmunoassay (RIA) for measuring isotype-specific antibodies to the myelin-associated glycoprotein (MAG) was developed using radiolabeled CNS MAG in a double-antibody precipitation system. Anti-MAG activity was detected by RIA only in patients with neuropathy and anti-MAG M proteins. Anti-MAG IgM or IgG antibodies were not detected in serum of patients with Guillain-Barré syndrome, chronic relapsing polyneuritis, or multiple sclerosis (MS). Some patients with anti-MAG IgM M proteins also had complexes of IgG or IgA bound to the M protein. In one patient, anti-CNS MAG activity was detected by RIA, but not by ELISA or immunoblot. Anti-MAG antibody activity in patients with neuropathy seems to be isotypically restricted, and there is no evidence for antibody reactivity to MAG in other demyelinating diseases.