β-Amyloid (1-42), human TFA
(Synonyms: 大豆肽) 目录号 : GC16243淀粉样蛋白 β 肽 (1-42) 人 TFA 是一种由 42 个氨基酸组成的肽。
Cas No.:107761-42-2
Sample solution is provided at 25 µL, 10mM.
Amyloid β-Peptide (1-42) human TFA is a 42-amino acid peptide. Alzheimer's disease (AD) is characterized phenotypically by memory impairment, neurochemically by accumulation of β-amyloid peptide (such as β-Amyloid (1-42)) and morphologically by an initial loss of nerve terminals in cortical and hippocampal regions [1]. the abnormal production of soluble forms of β-amyloid peptides (Aβ), such as β-Amyloid (1-42), have been proposed as a major culprit in AD [2].
β-Amyloid (1-42) can impair synaptic function, typified by its ability to affect synaptic plasticity [3], and trigger events leading to a loss of viability of synapses [4], and leads to memory impairment [5]. The intracerebroventricular administration of β-Amyloid (1-42) has been proposed as a model of AD [6].
β-Amyloid (1-42) (100 μg/ml) for 24 h cell viability ofSH-SY5Y cells dropped to about 50%, β-Amyloid (1-42)-induced cell apoptosis could be completely prevented by EGb761 at 100 μg/ml and to a lesser extent, by quercetin (1.5 μg/ml) and ginkgolide B (10 μg/ml) [7].
β-Amyloid (1-42) (icv. 2 nmol in 4 μl) caused a predominant loss of glutamatergic and cholinergic markers [1].β-Amyloid (1-42) was combined with inducers of oxidative stress to induce neuronal cell death, amyloid deposits, gliosis and memory impairment following a 4 week intracerebroventricular infusion. Oxidative stress was induced using the pro-oxidative cation Fe2+ and the glutathione synthesis inhibitor buthionine sulfoximine (BSO) [8].
References:
[1].Canas P M, Sim?es A P, Rodrigues R J, et al. Predominant loss of glutamatergic terminal markers in a β-amyloid peptide model of Alzheimer's disease[J]. Neuropharmacology, 2014, 76: 51-56.
[2].Hardy J, Selkoe D J. The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics[J]. science, 2002, 297(5580): 353-356.
[3].Venkitaramani D V, Chin J, Netzer W J, et al. β-amyloid modulation of synaptic transmission and plasticity[J]. Journal of Neuroscience, 2007, 27(44): 11832-11837.
[4].Mattson M P, Partin J, Begley J G. Amyloid β-peptide induces apoptosis-related events in synapses and dendrites[J]. Brain research, 1998, 807(1-2): 167-176.
[5].Selkoe D J. Soluble oligomers of the amyloid β-protein: Impair synaptic plasticity and behavior[J]. Synaptic Plasticity and the Mechanism of Alzheimer's Disease, 2008: 89-102.
[6].Lawlor P A, Young D. Aβ infusion and related models of Alzheimer dementia[M]//Animal models of Dementia. Humana Press, 2011: 347-370.
[7].Shi C, Zhao L, Zhu B, et al. Protective effects of Ginkgo biloba extract (EGb761) and its constituents quercetin and ginkgolide B against β-amyloid peptide-induced toxicity in SH-SY5Y cells[J]. Chemico-biological interactions, 2009, 181(1): 115-123.
[8].Lecanu, L., Greeson, J., & Papadopoulos, V. (2006). Beta-amyloid and oxidative stress jointly induce neuronal death, amyloid deposits, gliosis, and memory impairment in the rat brain. Pharmacology, 76(1), 19-33.
Cell experiment [1]: | |
Cell lines |
PC12, cerebral cortex neurons |
Preparation Method |
β-Amyloid (1-42), human TFA was dissolved in dimethyl sulfoxide (DMSO) at a concentration of 1 mM and pre-incubated at 37°C for 7 days to promote aggregation and then diluted in medium, then oligomerized β-Amyloid (1-42) (equivalent to 1 mM peptides) were prepared for β-Amyloid (1-42) insult experiments. For PC12 cellular AD model construction, PC12 cells were firstly cultured in 20 ng/ml nerve growth factor (NGF) and 10% FBS for 72 h at 37°C with 95% air and 5% CO2 to promote PC12 cells differentiation, and then 1 uM of oligomerized β-Amyloid (1-42) were added for 24 h to build PC12 cellular AD models. For cellular AD model of cerebral cortex neurons, 1 mM of oligomerized β-Amyloid (1-42) peptides was added in primary cerebral cortex neurons for 24 h to build cellular AD model of cerebral cortex neurons. |
Reaction Conditions |
1 uM for 24 h |
Applications |
Cell viability was reduced in β-Amyloid (1-42) insult group compared with a control group in NGF stimulated PC 12 cells and primary cerebral cortex neurons from rat embryo cells, indicating successes in the construction of cellular AD models. |
Animal experiment [2]: | |
Animal models |
Male Wistar rats weighing 210-230 g |
Preparation Method |
AD model was induced by β-Amyloid (1-42) dissolved in normal saline at the concentration of 4 µg/µl. The solution was kept at room temperature for 3 days before administration75. β-Amyloid (1-42) or saline was injected in a volume of 2 µl over 5 min via a microsyringe pump connected to the 25-gauge stainless steel needle bilaterally into the lateral cerebral ventricles according to stereotaxic coordination. |
Dosage form |
4 µg/µl, 2 µl, lateral cerebral ventricle injection |
Applications |
Immunostaining of β-Amyloid (1-42) of entorhinal cortex (EC), and dorsal hippocampus (dHPC) sections demonstrated a high level of Aβ plaques in β-Amyloid (1-42) animals compared to the saline group. |
References: [1]: Yang H, Wang H, Shang H, et al. Circular RNA circ_0000950 promotes neuron apoptosis, suppresses neurite outgrowth and elevates inflammatory cytokines levels via directly sponging miR-103 in Alzheimer's disease[J]. Cell Cycle, 2019, 18(18): 2197-2214. |
Cas No. | 107761-42-2 | SDF | |
别名 | 大豆肽 | ||
分子式 | C203H311N55O60S | 分子量 | 4514.08 |
溶解度 | Soluble to 1 mg/ml in 50mM Tris buffer | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 0.2215 mL | 1.1076 mL | 2.2153 mL |
5 mM | 0.0443 mL | 0.2215 mL | 0.4431 mL |
10 mM | 0.0222 mL | 0.1108 mL | 0.2215 mL |
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