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Publication : Cyanidin 3-O-β-glucopyranoside activates peroxisome proliferator-activated receptor-γ and alleviates cognitive impairment in the APP(swe)/PS1(ΔE9) mouse model.

First Author  Song N Year  2016
Journal  Biochim Biophys Acta Volume  1862
Issue  9 Pages  1786-800
PubMed ID  27240542 Mgi Jnum  J:255668
Mgi Id  MGI:6105301 Doi  10.1016/j.bbadis.2016.05.016
Citation  Song N, et al. (2016) Cyanidin 3-O-beta-glucopyranoside activates peroxisome proliferator-activated receptor-gamma and alleviates cognitive impairment in the APP(swe)/PS1(DeltaE9) mouse model. Biochim Biophys Acta 1862(9):1786-800
abstractText  Alzheimer''s disease (AD) is currently one of the most common neurodegenerative disorders worldwide. To date, no cure has been developed for AD, and some disease-modifying treatments show side effects and low efficacy. Increasing evidence shows that cyanidin 3-O-beta-glucopyranoside (Cy3G), which is naturally derived from many plants, may provide protection against neurodegenerative diseases including AD; however, its exact role is still unclear. Therefore, we investigated the mechanisms of the effects of Cy3G on beta-amyloid 25-35 (Abeta25-35)-induced SH-SY5Y cell injury and cognitive impairment in the APP(swe)/PS1(DeltaE9) (PAP) mouse model of AD. Furthermore, we aimed to determine the molecular target initiated by Cy3G. The data indicated that Cy3G-mediated neuroprotection involved the inhibition of Abeta25-35 binding to the cell surface and spontaneous aggregation of Abeta25-35 fibrils at the molecular level. Furthermore, in an in vitro study, Abeta25-35-mediated cytotoxicity, which was caused by inducing apoptotic cell death and ROS formation, was also ameliorated by Cy3G intervention. In addition, upregulation of peroxisome proliferator-activated receptor-gamma (PPARgamma) protein involved in glucose/lipid metabolism by Cy3G treatment verified that the initiated molecule was Cy3G. In an in vivo study, Cy3G was shown to alleviate cognitive impairment, improve cerebral glucose uptake and decrease fasting blood glucose levels. In conclusion, Cy3G ameliorates amyloid beta peptide-induced injury both in vitro and in vivo through the PPARgamma pathway. Thus, Cy3G has a good safety profile as a potential natural PPARgamma agonist and may be used as an ideal alternative to traditional disease-modifying treatments against AD.
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