MBP (68–86)髓鞘堿性蛋白（68–86）

產(chǎn)品關(guān)鍵詞：

MBP (68–86) ；MBP (87-99) ；MOG (35-55)髓鞘少突膠質(zhì)細胞糖蛋白（35-55）；中樞神經(jīng)系統（CNS）；Multiple Sclerosis (MS)多發(fā)性硬化癥；實(shí)驗性自身免疫性腦脊髓炎（EAE）；PLP (178-191)； 

產(chǎn)品信息

產(chǎn)品描述

MBP，英文全名Myelin Basic Protein，中文名髓鞘堿性蛋白或髓磷脂堿性蛋白，是構成中樞神經(jīng)系統（CNS）髓磷脂的重要成分，由少突膠質(zhì)細胞和施萬(wàn)細胞（Schwann cells）合成，可用作這兩種細胞的標記物。MBP是一條單鏈多肽，分子量約18.5kDa，位于致密的髓鞘和髓核中。是一種有潛力的靶向抗原，能夠誘發(fā)動(dòng)物產(chǎn)生實(shí)驗性過(guò)敏性腦脊髓炎（EAE）。MBP的致腦炎肽隨敏感品系不同而有差異，且與MHC Class II基因型有關(guān)。

產(chǎn)品特性

1） 同義名：Myelin Basic Protein peptide (68–86); 髓鞘堿性蛋白肽段（68-86）；

2） 分子式：C81H129N25O30

3） 分子量：1933.1

4） 純度：≥95%（HPLC）

5） 外觀(guān)：白色至類(lèi)白色凍干粉

6） 溶解性：溶于水（1 mg/ml）

7） 單字母序列：YGSLPQKSQRSQDENPV

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

保存與運輸方法

保存：-20 °C干燥保存，一年有效。

運輸：冰袋運輸。

注意事項

1） 本品以?xún)龈煞坌问教峁?，可能因量少不易觀(guān)察到。請直接加溶劑到瓶子內，低速漩渦震蕩以確保充分溶解；制備好的儲存液，根據單次用量分裝，置于-20°C避光凍存，避免反復凍融。

2） 本品的抗衡離子是三氟乙酸（TFA）；

3） 為了您的安全和健康，請穿實(shí)驗服并戴一次性手套操作。

應用示例（來(lái)自文獻，僅做參考）

1）文獻來(lái)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. https://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）文獻來(lái)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【版權歸MKBio懋康所有】

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