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Protective Role Of Naringenin Against Aβ25-35-Caused Damage via ER and PI3K/Akt-Mediated Pathways

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Abstract

Senile plaque accumulation and neurofibrillary tangles are primary characteristics of Alzheimer’s disease. We aimed to assess the protective functions of naringenin against β-amyloid protein fragment 25-35 (Aβ25-35)-caused nerve damage in differentiated PC12 cells, and study the potential mechanisms. We evaluated cell viability and apoptosis using the 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) test and flow cytometry, respectively. Moreover, we measured protein kinase B (Akt), glycogen synthase kinase-3β (GSK-3β), and caspase-3 activity via western blotting and RT-PCR. We found that naringenin protected cell against Aβ25-35-caused nerve damage by increasing cell viability, promoting Akt and GSK3β activation, and inhibiting cell apoptosis and caspase-3 activity. However, treatment with the estrogen receptor (ER) antagonist ICI182, 780 or phosphatidylinositol-3-kinase (PI3K) inhibitor LY294002 suppressed the effects of naringenin. Our results suggested that naringenin could effectively suppress Aβ25-35-caused nerve damage in PC12 cells by regulating the ER and PI3K/Akt pathways.

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Acknowledgements

This work was supported by National Natural Science Foundation of China (General Program, Grant No. 81673581), Harbin science and technology innovation talent research special funds (rqyxj012 outstanding youth talent, 2016), and Heilongjiang university of Chinese medicine scientific research fund (2015 xy04).

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Correspondence to Xiuhong Wu or Fang Geng.

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Zhang, N., Hu, Z., Zhang, Z. et al. Protective Role Of Naringenin Against Aβ25-35-Caused Damage via ER and PI3K/Akt-Mediated Pathways. Cell Mol Neurobiol 38, 549–557 (2018). https://doi.org/10.1007/s10571-017-0519-8

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