COG 133
(Synonyms: Leu-Arg-Val-Arg-Leu-Ala-Ser-His-Leu-Arg-Lys-Leu-Arg-Lys-Arg-Leu-Leu ) 目录号 : GP10010
A peptide fragment of ApoE and an α7 nAChR antagonist
Cas No.:514200-66-9
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
|
Cell lines |
IEC-6 cell monolayers |
|
Preparation method |
Soluble to 1 mg/ml in sterile water. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
|
Reacting condition |
0.02, 0.2, 2, 5, 10, and 20 μM, 24 h |
|
Applications |
COG 133 (0.02, 0.2, and 2.0 μM) improved cell numbers in glutamine free media. In IEC-6 cells, COG 133 (0.2-20 μM) improved cell migration following 5-FU challenge, reaching the same migration level as controls. |
| Animal experiment [1]: | |
|
Animal models |
5-fluorouracil (5-FU)-challenged Swiss mice, C57BL6J ApoE knock-out mice |
|
Dosage form |
Intraperitoneal injection, 0.3, 1, and 3 μM, twice daily for 4 days |
|
Application |
COG 133 (3 μM) significantly increased the mitotic crypt numbers in C57BL6J wild-type animals. COG 133 treatment improved crypt architecture and reduced lamina propria inflammation. COG 133 (3 μM) significantly reduced the intestinal MPO levels. COG 133 partially decreased TNF-α level in the proximal small intestine from 5-FU-treated mice. In both wild-type and ApoE knock-out mice, COG 133 (3 μM) reverted the increase in Tunel-positive cells in the proximal intestine induced by 5-FU. COG 133 caused higher expression of the NF-κB in the improved intestinal mucosa. |
|
Other notes |
Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
|
References: [1]. Azevedo O G R, Oliveira R A C, Oliveira B C, et al. Apolipoprotein E COG 133 mimetic peptide improves 5-fluorouracil-induced intestinal mucositis[J]. BMC gastroenterology, 2012, 12(1): 35. |
|
COG 133, (C97H181N37O19), a peptide with the sequence Ac-Leu-Arg-Val-Arg-Leu-Ala-Ser-His-Leu-Arg-Lys-Leu-Arg-Lys-Arg-Leu-Leu-amide,MW= 2169.73.Apolipoprotein E (ApoE) is 299 amino acids long and transports lipoproteins1, fat-soluble vitamins, and cholesterol into the lymph system and then into the blood. It is synthesized principally in the liver, but has also been found in other tissues such as the brain, kidneys, and spleen. In the nervous system, non-neuronal cell types, most notably astroglia and microglia, are the primary producers of APOE, while neurons preferentially express the receptors for APOE. There are seven currently identified mammalian receptors for APOE which belong to the evolutionarily conserved low density lipoprotein receptor gene family.APOE was initially recognized for its importance in lipoprotein metabolism and cardiovascular disease2. Defects in APOE result in familial dysbetalipoproteinemia aka type III hyperlipoproteinemia (HLP III), in which increased plasma cholesterol and triglycerides are the consequence of impaired clearance of chylomicron, VLDL and LDL remnants[citation needed]. More recently, it has been studied for its role in several biological processes not directly related to lipoprotein transport, including Alzheimer's disease (AD), immunoregulation, and cognition3.
References:
1. Singh PP, Singh M, Mastana SS (2002). "Genetic variation of apolipoproteins in North Indians". Hum. Biol. 74 (5): 673-82.
2. van den Elzen P, Garg S, LeȮn L, Brigl M, Leadbetter EA, Gumperz JE, Dascher CC, Cheng TY, Sacks FM, Illarionov PA, Besra GS, Kent SC, Moody DB, BrennerMB. (2005). "Apolipoprotein-mediated pathways of lipid antigen presentation.". Nature 437 (7060): 906-10.
3. Zhang HL, Wu J, Zhu J (2010). "The Role of Apolipoprotein E in Guillain-BarrȦ Syndrome and Experimental Autoimmune Neuritis". J. Biomed. Biotechnol. 2010: 357412.
| Cas No. | 514200-66-9 | SDF | |
| 别名 | Leu-Arg-Val-Arg-Leu-Ala-Ser-His-Leu-Arg-Lys-Leu-Arg-Lys-Arg-Leu-Leu | ||
| 分子式 | C97H181N37O19 | 分子量 | 2169.73 |
| 溶解度 | ≥ 217mg/mL in DMSO; ≤1mg/ml in Water (Need ultrasonic) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 0.4609 mL | 2.3044 mL | 4.6089 mL |
| 5 mM | 0.0922 mL | 0.4609 mL | 0.9218 mL |
| 10 mM | 0.0461 mL | 0.2304 mL | 0.4609 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Apolipoprotein E COG 133 mimetic peptide improves 5-fluorouracil-induced intestinal mucositis
Background: Intestinal mucositis is one of the major troublesome side effects of anticancer chemotherapy leading to poor patient compliance. In this study we addressed the role of the novel apolipoprotein E (ApoE) COG 133 mimetic peptide in 5-fluorouracil (5-FU)-challenged Swiss mice and IEC-6 cell monolayers. Experiments were also conducted in C57BL6J ApoE knock-out mice to assess the effects of apoE peptide treatment.
Methods: Experimental groups were as follows: unchallenged controls, 5-FU-challenged mice (450 mg/kg, i.p) with or without the ApoE peptide (0.3, 1, and 3 μM, given twice daily i.p. for 4 days). Mice were sacrificed 3 days after 5-FU challenge. Proximal small intestinal samples were harvested for molecular biology and histological processing. We conducted ELISA assays and RT-PCR to target IL-1β, TNF-α, IL-10, iNOS, and myeloperoxidase (MPO) to assess intestinal inflammation. Cell death and NF-κB assays were also conducted in apoE knock-out mice. In our in vitro models, IEC-6 cells were exposed to 1 mM of 5-FU in glutamine free media with or without the ApoE peptide (0.02, 0.2, 2, 5, 10, and 20 μM). We investigated IEC-6 cell proliferation and migration, 24 h after the 5-FU challenge. Additionally, apoptotic IEC-6 cells were measured by Tunel and flow cytometry. Equimolar doses of the ApoA-I (D4-F) peptide were also used in some experiments for comparative studies.
Results: Villus blunting and heavy inflammatory infiltrates were seen in the 5-FU-challenged group, findings that were partially ameliorated by the ApoE peptide. We found increased intestinal MPO and pro-inflammatory IL-1β and TNF-α levels, and TNF-α and iNOS transcripts, and reduction of IL-10 following 5-FU treatment, each of which were partially abrogated by the peptide. Improvements were also found in IEC-6 cell apoptosis and migration following ApoE and D-4F treatment.
Conclusion: Altogether, these findings suggest that the novel ApoE COG 133 mimetic peptide can reduce 5-FU-induced intestinal changes and potentially benefit mucositis.