http://www.cnr.it/ontology/cnr/individuo/prodotto/ID17422
Protective effect of rhubarb derivatives on amyloid beta (1-42) peptide-induced apoptosis in IMR-32 cells: A case of nutrigenomic (Articolo in rivista)
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- Protective effect of rhubarb derivatives on amyloid beta (1-42) peptide-induced apoptosis in IMR-32 cells: A case of nutrigenomic (Articolo in rivista) (literal)
- Anno
- 2006-01-01T00:00:00+01:00 (literal)
- Alternative label
Misiti F., Sampaolese B., Mezzogori D., Orsini F., Pezzotti A., Giardina B., Clementi M.E. (2006)
Protective effect of rhubarb derivatives on amyloid beta (1-42) peptide-induced apoptosis in IMR-32 cells: A case of nutrigenomic
in Brain research bulletin
(literal)
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- Misiti F., Sampaolese B., Mezzogori D., Orsini F., Pezzotti A., Giardina B., Clementi M.E. (literal)
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- F. Misiti, Department of Health and Motor Sciences, University of Cassino, V.le Bonomi, 03043 Cassino (FR), Italy
B. Sampaolese, CNR-ICRM, Institute of \"Chimica del Riconoscimento Molecolare\", c/o Institute of Biochemistry and Clinical Biochemistry, Faculty of Medicine, Catholic University School of Medicine, Largo F. Vito 1, 00168 Rome, Italy
D. Mezzogori, Institute of Physiology, Catholic University School of Medicine, Largo F. Vito 1, 00168 Rome, Italy
F. Orsini Institute of Biochemistry and Clinical Biochemistry, Faculty of Medicine, Catholic University School of Medicine, Largo F. Vito 1, 00168 Rome, Italy
M. Pezzotti Institute of Biochemistry and Clinical Biochemistry, Faculty of Medicine, Catholic University School of Medicine, Largo F. Vito 1, 00168 Rome, Italy
B. Giardina CNR-ICRM, Institute of \"Chimica del Riconoscimento Molecolare\", Institute of Biochemistry and Clinical Biochemistry, Faculty of Medicine, Catholic University School of Medicine, Largo F. Vito 1, 00168 Rome, Italy
M.E. Clementi CNR-ICRM, Institute of \"Chimica del Riconoscimento Molecolare\", Institute of Biochemistry and Clinical Biochemistry, Faculty of Medicine, Catholic University School of Medicine, Largo F. Vito 1, 00168 Rome, Italy (literal)
- Titolo
- Protective effect of rhubarb derivatives on amyloid beta (1-42) peptide-induced apoptosis in IMR-32 cells: A case of nutrigenomic (literal)
- Abstract
- Amyloid beta (1-42) peptide is considered responsible for the formation of senile plaques that accumulate in the brains of patients with
Alzheimer's disease (AD). In the last years considerable attention has been focused on identifying natural food products, such as phytochemicals
that prevent or almost retard the appearance of amyloid beta (1-42)-related neurotoxic effects. In this study, human neuroblastoma cells (IMR-
32) was used as system model to evaluate the protective role of rhaponticin (3,3?,5-trihydroxy-4?-methoxystilbene 3-O-d-glucoside) a stilbene
glucoside extracted from rhubarb roots (Rhei rhizoma) and rhapontigenin, its aglycone metabolite, against amyloid beta (1-42)-dependent toxicity.
The obtained results show that rhapontigenin maintains significant cell viability in a dose-dependent manner and it exerts a protective effect on
mitochondrial functionality, as evidenced by mitochondrial oxygen consumption experiments. A similar behaviour, but to a lesser extent, has been
shown by rhaponticin.
The protective mechanism mediated by the two stilbenes could be related to their effect on bcl-2 gene family expression. Bax, a pro-apoptotic gene,
resulted down-regulated by the treatment with rhaponticin and rhapontigenin compared with the results obtained in the presence of amyloid beta
(1-42) peptide. Conversely, bcl-2, an anti-apoptotic gene, highly down-regulated by amyloid beta (1-42) treatment, resulted expressed in the presence
of stilbenes similarly to that shown by control cells. The obtained results support the hypothesis that amyloid beta (1-42)-induced neurotoxicity
occurs via bax over-expression, bcl-2 down-regulation, firstly indicating that rhaponticin and its aglycone moiety may alter this cell death pathway.
Based on these studies, we suggest that rhaponticin and its main metabolite could be developed as agents for the management of AD. (literal)
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