规格: | 98% |
分子量: | 4385.7 |
包装 | 价格(元) |
1mg | 电议 |
5mg | 电议 |
Background:
Neuropeptide Y (29-64), amide, human (TFA) is involved in Alzheimer's disease (AD) and protects rat cortical neurons against β-Amyloid toxicity.
It is showed that Neuropeptide Y (29-64), amide, human (TFA) is able to protect cortical neurons from Aβ25-35 toxicity. 2 μM NPY abolishes the toxic effects of Aβ25-35 at 24 and 48 h. The same effect on neuronal survival is observed in neurons exposed to 1 μM and 0.5 μM Neuropeptide Y (29-64), amide, human (TFA) pretreatments. Pretreatment with Neuropeptide Y (29-64), amide, human (TFA) Increases NGF Synthesis, reduces NGF mRNA, and restores NGF release in cortical neurons exposed to Aβ35-25[1].
[1]. Croce N, et al. Neuropeptide Y protects rat cortical neurons against β-amyloid toxicity and re-establishes synthesis and release of nerve growth factor. ACS Chem Neurosci. 2012 Apr 18;3(4):312-8.
Protocol:
Cell experiment: | Primary cortical neurons are preincubated either alone (positive control) or with three concentrations of Neuropeptide Y (29-64), amide, human (TFA) (NPY) (0.5, 1, and 2 μM) for 24 h and then exposed to Aβ25-35 (50 μM) or Aβ35-25 (50 μM) for 48 h[1]. |
参考文献: [1]. Croce N, et al. Neuropeptide Y protects rat cortical neurons against β-amyloid toxicity and re-establishes synthesis and release of nerve growth factor. ACS Chem Neurosci. 2012 Apr 18;3(4):312-8. |