GLPBio

Amyloid Beta-Peptide (1-40) (human)

Catalog No.: GP10118Purity:>96.00%
COASDSData Sheet

Amyloid β-Peptid (1-40) (human), (C194H295N53O58S1), ist ein Peptid mit der Sequenz H2N-DAEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVVIA-OH, MW= 4329.8. Amyloid-Beta (Aβ oder Abeta) ist ein Peptid von 36–43 Aminosäuren, das aus dem Amyloid-Vorläuferprotein verarbeitet wird.

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Amyloid Beta-Peptide (1-40) (human)
Cas No.: 131438-79-4
1mgIn Stock
$91.00
1
5mgIn Stock
$263.00
1
10mgIn Stock
$453.00
1
25mgIn Stock
$625.00
1
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Zitate (Citations)

1 publicationsPublikationen von Forschern, die dieses Produkt verwenden
IF 10

Beschreibung (Description)

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.

Protokoll (Protocol)

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:
[1] 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.
[2] 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.

Produktdokumente (Product Documents)

Purity:>96.00%Appearance:A solid
COASDSData Sheet

Chemische Eigenschaften (Chemical Properties)

CAS-Nr.
131438-79-4
Summenformel
C194H295N53O58S
Molekulargewicht
4329.86
Löslichkeit
≥43.28mg/mL in DMSO
Lagerung
Desiccate at -20°C
Allgemeine Hinweise
Wählen Sie anhand der Löslichkeitsdaten des Produkts ein geeignetes Lösungsmittel. Aliquotieren Sie die Stammlösung nach der Herstellung, um wiederholte Gefrier-Auftau-Zyklen zu vermeiden.
Verwenden Sie Stammlösungen bei Lagerung bei -80°C innerhalb von 6 Monaten bzw. bei -20°C innerhalb von 1 Monat.
Zur Verbesserung der Löslichkeit das Röhrchen auf 37°C erwärmen und für eine angemessene Dauer beschallen.
Versandbedingungen
Evaluierungsmuster werden mit Kühlakkus versandt. Andere verfügbare Größen werden bei Raumtemperatur oder auf Anfrage mit Kühlakkus versandt.

Rechner (Calculators)Molarität / Verdünnung / Molekulargewicht / Einheitenumrechnung / In-vivo-Formulierung / Löslichkeit

g/mol

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