Amyloid Beta-Peptide (1-40) (human)
(Synonyms: BETA淀粉样蛋白片段1-40,Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val ) 目录号 : GP10118
Amyloid Beta-Peptide (1-40) (human)是老年斑淀粉样蛋白的主要成分，作为生理性肽段存在于脑组织、脑脊液（CSF）及血浆中。
Cas No.:131438-79-4
Sample solution is provided at 25 µL, 10mM.
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Amyloid Beta-Peptide (1-40) (human) is the main component of senile plaque amyloid and is a physiological peptide present in the brain, cerebrospinal fluid (CSF), and plasma[1]. Amyloid Beta-Peptide (1-40) has been used to establish animal models for investigating the study of neuronal survival[2].
In vitro, 200nM of Amyloid Beta-Peptide (1-40) treatment of CA1 pyramidal cells for 20 minutes can increase the barium current (IBa) to 1.74[3]. Treatment with 30μM Amyloid Beta-Peptide (1-40) for 24 hours caused an increase in the release of nitric oxide (NO) and tumor necrosis factor alpha (TNF-α) in primary microglial cells of mice, promoting inflammation response[4].
In vivo, a single intrahippocampal injection of 2μl of Amyloid Beta-Peptide (1-40) (5μg/μl) resulted in a continuous decline in the spatial memory and learning ability of rats over a period of 5 days. Injecting 2.5μL of 800μM Amyloid Beta-Peptide (1-40) into the entorhinal cortex of rats can prevent the hyperphosphorylation of tau of tau in the rat hippocampus caused by Aβ1-42, and protect the neurons in the rat brain from damage caused by Aβ1-42[6].
References:
[1] Chen G, Xu T, Yan Y, et al. Amyloid beta: structure, biology and structure-based therapeutic development[J]. Acta pharmacologica sinica, 2017, 38(9): 1205-1235.
[2] Nitta A, Itoh A, Hasegawa T, et al. β-Amyloid protein-induced Alzheimer's disease animal model[J]. Neuroscience letters, 1994, 170(1): 63-66.
[3] Rovira C, Arbez N, Mariani J. Aβ (25–35) and Aβ (1–40) act on different calcium channels in CA1 hippocampal neurons[J]. Biochemical and biophysical research communications, 2002, 296(5): 1317-1321.
[4] Lotz M, Ebert S, Esselmann H, et al. Amyloid beta peptide 1–40 enhances the action of Toll‐like receptor‐2 and‐4 agonists but antagonizes Toll‐like receptor‐9‐induced inflammation in primary mouse microglial cell cultures[J]. Journal of neurochemistry, 2005, 94(2): 289-298.
[5] Shi X, Lu X, Zhan L, et al. Rat hippocampal proteomic alterations following intrahippocampal injection of amyloid beta peptide (1–40)[J]. Neuroscience letters, 2011, 500(2): 87-91.
[6] Zou K, Kim D, Kakio A, et al. Amyloid β‐protein (Aβ) 1–40 protects neurons from damage induced by Aβ1–42 in culture and in rat brain[J]. Journal of neurochemistry, 2003, 87(3): 609-619.
Amyloid Beta-Peptide (1-40) (human)是老年斑淀粉样蛋白的主要成分，作为生理性肽段存在于脑组织、脑脊液（CSF）及血浆中[1]。Amyloid Beta-Peptide (1-40)已被用于建立动物模型来研究神经元的存活[2]。
在体外，200nM浓度的Amyloid Beta-Peptide (1-40)处理CA1锥体神经元细胞20分钟，可使钡电流（IBa）增强至1.74[3]。10μM浓度的Amyloid Beta-Peptide (1-40)处理小鼠原代小胶质细胞24小时，能促进一氧化氮（NO）和肿瘤坏死因子α（TNF-α）释放，加剧炎症反应[4]。
在体内，大鼠海马单次注射2μL的Amyloid Beta-Peptide (1-40)（5μg/μL）可导致大鼠的空间记忆与学习能力持续5天进行性衰退[5]。 向大鼠内嗅皮层注射2.5μL 800μM Amyloid Beta-Peptide (1-40)，能阻止Aβ1-42诱导的海马区tau蛋白过度磷酸化，保护脑神经元免受Aβ1-42损伤[6]。
| Cell experiment [1]: | |
Cell lines | Primary mouse microglial cells |
Preparation Method | The primary mouse microglial cells were suspended in the modified Eagle's Modified Essential Medium (DMEM) supplemented with glutamine, 10% fetal bovine serum (FCS), 100U/mL penicillin, and 100μg/mL streptomycin. The cells were inoculated at a density of 2 microglial cells per 75 cubic centimeter flask from 2 brain tissues, and cultured in a humidified environment at 37°C with 5% CO2. The medium was changed twice a week. After 10-14 days, a confluent mixed glial cell cluster was formed and oscillated at a speed of 200 times per minute for 30 minutes. The microglial cells isolated from the supernatant were re-inoculated in 96-well cell culture plates, with 75,000 cells per well. Three hours later, the microglial cells were exposed to different TLR agonists and Amyloid Beta-Peptide (1-40) (human), with interferon-c (100U/mL) present for 24 hours. The TLR agonists stimulated the microglial cells for less than 24 hours caused mild or no response. The stock solution of Amyloid Beta-Peptide (1-40) (human) (concentration of 1mM) was diluted into the cell culture medium (containing glutamine, 10% fetal bovine serum, 100units/mL penicillin, and 100mg/mL streptomycin) to a final concentration of 0, 1, 10 and 30μM. The control group was only treated with the medium and interferon-C. The supernatants extracted from the stimulated glial cell cultures and the unstimulated control group were directly used to detect the production of nitric oxide (NO), or were frozen at -80℃ until the levels of tumor necrosis factor alpha (TNF-α) were measured. |
Reaction Conditions | 0, 1, 10 and 30μM; 24h |
Applications | Amyloid Beta-Peptide (1-40) dose-dependently increased the release of nitric oxide NO and TNF-α in primary mouse microglial cells. |
| Animal experiment [2]: | |
Animal models | Male Wistar rat |
Preparation Method | Eight-week-old male Sprague-Dawley laboratory rats, weighing between 200 and 220 grams, were placed in plastic cages. The rats were provided with sufficient food and water, and were housed at a room temperature of 21-23℃, following a 12-hour light/dark cycle. Dissolve the Amyloid Beta-Peptide (1-40) (human) in distilled water at a concentration of 5μg/μl, and incubate at 37 ℃ for 7 days before use. First, the rats were anesthetized with pentobarbital sodium (45mg/kg; i.p), and placed in the stereotactic apparatus. Next, a cut was made on the scalp and the scalp was lifted upwards. Then, a hole was drilled on the skull using a dental drill. The stereotactic coordinates were: anterior-posterior (AP) = -3.5mm, medial-lateral (ML) = 2.0mm, dorsal-ventral (DV) = 2.7mm, starting from the Brodmann point. 14 rats were randomly divided into two groups: (1) rats injected with pure water as the control group, (2) rats injected with Amyloid Beta-Peptide (1-40) as the Aβ1-40 group. 2μl Amyloid Beta-Peptide (1-40) or distilled water was injected at a flow rate of 0.5μl/min. After the injection, the needle was kept in the original position for 5 minutes, and then slowly withdrawn. The behavioral performances of animals were assessed by the step-down passive avoidance test and Morris water maze test over a period of 5 days. |
Dosage form | 5μg/μl, 2μl for once; i.c.v |
Applications | Injections of Amyloid Beta-Peptide (1-40) into the brain can lead to a decline in the spatial memory and learning abilities of rats. |
References: | |
| Cas No. | 131438-79-4 | SDF | |
| 别名 | BETA淀粉样蛋白片段1-40,Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val | ||
| 分子式 | C194H295N53O58S | 分子量 | 4329.86 |
| 溶解度 | ≥ 43.28mg/mL in DMSO | 储存条件 | Desiccate 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。 |
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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.231 mL | 1.1548 mL | 2.3095 mL |
| 5 mM | 0.0462 mL | 0.231 mL | 0.4619 mL |
| 10 mM | 0.0231 mL | 0.1155 mL | 0.231 mL |
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| 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 | ||||||||||
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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，
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2.
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