Reply #5: I have the link, but please cover your eyes and try not to see the [View All]

[HysteryDiagnosis]

ads for the products on this page, just read the article... sorry to hear. You may want to look up curcumin, tumeric and certainly pycnogenol.

http://www.lef.org/news/LefDailyNews.htm?NewsID=6556&Section=Aging


http://www.ncbi.nlm.nih.gov/pubmed/12117551?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
1: Brain Res Mol Brain Res. 2002 Jul 15;104(1):55-65.Click here to read Links
Pycnogenol protects neurons from amyloid-beta peptide-induced apoptosis.
Peng QL, Buz'Zard AR, Lau BH.

Department of Microbiology and Molecular Genetics, School of Medicine, Loma Linda University, Loma Linda, CA 92350, USA.

Neuronal apoptosis is one of the pathological features of Alzheimer's disease (AD). Morphological pathology reveals that neuronal apoptosis is associated with senile plaques containing amyloid-beta peptide (Abeta) in AD brains. Reactive oxygen species (ROS) has been proposed to be involved in the apoptotic mechanism of Abeta-mediated neurotoxicity. In the present study, using a rat pheochromocytoma (PC12) cell line, we investigated the effect of Pycnogenol (PYC), a potent antioxidant and ROS scavenger, on Abeta(25-35)-induced apoptosis and ROS generation. We used vitamin E, a known antioxidant agent, to verify the effect of PYC. Abeta(25-35)-induced apoptosis in PC12 cells was demonstrated by: (1) a dose-dependent loss of cell viability; (2) a time- and dose-dependent increase in the apoptotic cells; (3) an induction of DNA fragmentation; and (4) an increase in caspase-3 activity and cleavage of poly (ADP-ribose) polymerase (PARP). Our data showed that a significant increase in ROS formation preceded apoptotic events after PC12 cells were exposed to Abeta(25-35). We further found that PYC not only suppressed the generation of ROS but also attenuated caspase-3 activation, DNA fragmentation, PARP cleavage, and eventually protected against Abeta-induced apoptosis. Vitamin E also suppressed cell death and caspase-3 activation induced by Abeta(25-35). Taken together, these results suggest that ROS may be involved in Abeta-induced apoptosis in PC12 cells. They further suggest that PYC can reduce apoptosis, possibly by decreasing free radical generation in PC12 cells.

PMID: 12117551


1: Biol Pharm Bull. 2000 Jun;23(6):735-7.Links
Pycnogenol protects vascular endothelial cells from beta-amyloid-induced injury.
Liu F, Lau BH, Peng Q, Shah V.

Department of Microbiology and Molecular Genetics, School of Medicine, Loma Linda University, CA 92350, USA.

The neuropathological hallmarks of Alzheimer's disease (AD) are senile plaques, cerebrovascular beta-amyloidosis, neurofibrillary tangles, and selective neuronal loss. Beta-amyloid (Abeta) has been shown to cause vascular damage mediated by generation of reactive oxygen species and this damage is considered an early event in the development of AD. In this study, we determined the effect of pyenogenol, a potent antioxidant phytochemical, on Abeta-induced cellular injury. Pulmonary artery endothelial cells (PAEC) were exposed to Abeta for 24 h. Cell injury was assessed by measuring cell viability with methylthiazol tetrazolium (MTT) assay, and by determining the release of intracellular lactate dehydrogenase (LDH). Lipid peroxidation products of PAEC were determined by measuring thiobarbituric acid-reactive substances (TBARS). Exposure of PAEC to Abeta resulted in a decrease in cell viability, an increase of LDH release indicating membrane damage, and an elevated level of TBARS. Preincubation of PAEC with pycnogenol significantly minimized these changes. This study demonstrated that pycnogenol can protect vascular endothelial cells from Abeta-induced injury. The data suggest that pycnogenol may be useful for the prevention and/or treatment of vascular or neurodegenerative diseases associated with Abeta toxicity.

PMID: 10864026