MBP (68–86)髓鞘碱性蛋白 蛋白纯化

MBP (68–86)髓鞘碱性蛋白（68–86）

产品关键词：

MBP (68–86) ；MBP (87-99) ；MOG (35-55)髓鞘少突胶质细胞糖蛋白（35-55）；中枢神经系统（CNS）；Multiple Sclerosis (MS)多发性硬化症；实验性自身免疫性脑脊髓炎（EAE）；PLP (178-191)； 

产品信息

产品描述

MBP，英文全名Myelin Basic Protein，中文名髓鞘碱性蛋白或髓磷脂碱性蛋白，是构成中枢神经系统（CNS）髓磷脂的重要成分，由少突胶质细胞和施万细胞（Schwann cells）合成，可用作这两种细胞的标记物。MBP是一条单链多肽，分子量约18.5kDa，位于致密的髓鞘和髓核中。是一种有潜力的靶向抗原，能够诱发动物产生实验性过敏性脑脊髓炎（EAE）。MBP的致脑炎肽随敏感品系不同而有差异，且与MHC Class II基因型有关。

产品特性

1） 同义名：Myelin Basic Protein peptide (68–86); 髓鞘碱性蛋白肽段（68-86）；

2） 分子式：C81H129N25O30

3） 分子量：1933.1

4） 纯度：≥95%（HPLC）

5） 外观：白色至类白色冻干粉

6） 溶解性：溶于水（1 mg/ml）

7） 单字母序列：YGSLPQKSQRSQDENPV

8） 三字母序列：Tyr-Gly-Ser-Leu-Pro-Gln-Lys-Ser-Gln-Arg-Ser-Gln-Asp-Glu-Asn-Pro-Val

保存与运输方法

保存：-20 °C干燥保存，一年有效。

运输：冰袋运输。

注意事项

1） 本品以冻干粉形式提供，可能因量少不易观察到。请直接加溶剂到瓶子内，低速漩涡震荡以确保充分溶解；制备好的储存液，根据单次用量分装，置于-20°C避光冻存，避免反复冻融。

2） 本品的抗衡离子是三氟乙suan（TFA）；

3） 为了您的安全和健康，请穿实验服并戴一次性手套操作。

应用示例（来自文献，仅做参考）

1）文献来源：Liu Y, Wang H, Wang X, Mu L, Kong Q, Wang D, et al. (2013) The Mechanism of Effective Electroacupuncture on T Cell Response in Rats with Experimental Autoimmune Encephalomyelitis. PLoS ONE 8(1): e51573.    doi.org/10.1371/journal.pone.0051573

EAE模型建立：Myelin basic protein (MBP68–86) (YGSLPQKSQRSQDENPV) peptide 

Animals were divided into 4 treatment groups: (1) CFA emulsified in phosphate buffered saline (PBS) (CFA contained M. tuberculosis strain R37RA at a concentration of 20 mg/ml), (2) the EAE group consisted of rats immunized subcutaneously in the tail with 0.2 ml of 0.025 mg MBP68–86 emulsified in CFA, (3) the Zusanli acupoint (EA) immunization group that was immunized as group 2 but treated with EA, and (4) the NAL group that consisted of animals injected with naloxone (0.4 mg/kg) intravenously after electroacupuncture in 30 min. Prior to delivery, naloxone was diluted in sterile saline so that a 100 µl injection contained 250 µg of the drug. The Zusanli acupoint (ST36) is located 5 mm ventral and lateral to the anterior tubercle of the tibia. EA stimulation was applied for 30 min, started on the day of immunization, and repeated each day for a period of 21 days. Rats were scored for EAE as follows: 0, no disease; 1, piloerection; 2, loss in tail tonicity; 3, hind leg paralysis; 4, paraplegia, and 5, moribund or dead. Mean clinical scores at separate days and mean maximal scores were calculated by adding scores of individual rats and dividing by number of rats in each group.

2）文献来源：Xiao BG, Huang YM, Yang JS, Xu LY, Link H. Bone marrow-derived dendritic cells from experimental allergic encephalomyelitis induce immune tolerance to EAE in Lewis rats. Clin Exp Immunol. 2001 Aug;125(2):300-9. doi: 10.1046/j.1365-2249.2001.01573.x. PMID: 11529923; PMCID: PMC1906114.

EAE模型建立：Guinea pig MBP 68–86 (YGSLPQKSQRSQDENPV) 

EAE was induced for two purposes: (i) to incite pulsing of DC in vivo with autoantigen and (ii) to observe the effects of EAE-DC-induced tolerance to EAE. Lewis rats were immunized in both hind footpads with 200 µl of inoculum containing 25 µg of MBP 68–86, 2 mg Mycobacterium tuberculosis (strain H37RA; Difco, Detroit, MI), 100 µl saline and 100 µl Freund's incomplete adjuvant (Difco). On day 7 post-immunization (p.i.), BM DC representing ‘in vivo pulsed DC’ were prepared.

For the clinical evaluation of EAE and DC-induced tolerance to EAE, clinical scores of EAE were graded as follows: 0, asymptomatic; 1, loss of distal half of tail tonicity; 2, loss of entire tail tonicity; 3, hindlimb paresis; 4, hindlimb paralysis; 5, tetraplegia. Clinical observations of EAE were made blind by at least two investigators. All immunized animals injected with PBS (group I) developed clinical signs of EAE, with maximum symptoms around day 14 p.i., followed by clinical improvement and recovery on day 20 p.i. (Fig. 2a).

 — —Written/Edited by V. Shallan【版权归MKBio懋康所有】

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MBP (68–86)髓鞘碱性蛋白 蛋白纯化MBP (68–86)髓鞘碱性蛋白 蛋白纯化