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Post by beebs on May 9, 2012 6:39:04 GMT -5
Polyphenols and neuroprotection against ischemia and neurodegeneration.Lin B. Source Department of Neurology, University of Miami, Miller School of Medicine, Miami, Florida, USA. blin@med.miami.edu Abstract Neuroprotection of polyphenols in medical plants is getting attention in the world. Scutellaria baicalensis, paeonia veitchii and paeonia suffruticosa have been extensively studied in the last 10 years and show multi-function. They are neuroprotectants, antioxidants, anti-inflammatory and antithrombic agents as well as vasoconstriction inhibitors and amyloid-peptide (Aβ) cleaners by means of their polyphenols: baicalin, baicalein, wogonin (in scutellaria), and paeonol, paeonoside, paeoniflorin (PF) and 1, 2, 3, 4, 6-Penta-O-galloyl-beta-D-glucose (PGG) (in paeonia veitchii and paeonia suffruticosa). Other 4 medical plants: astragali, ligusticum wallichii, angelica sinensis and carthamus tinctorius (saffron) have been the major medicines to treat ischemia for hundreds of years in China, Korea and Japan. Our recent experimental studies demonstrated the neuroprotective efficacy of the combination of these phyotmedicines on mitigating brain infarction and global ischemia as well as preventing the neurodegeneration following ischemia. Owing to their multi-function, including improving cerebral blood circulation, they therefore have the potential to alleviate the symptoms of degenerative diseases, Alzheimer's disease (AD) and Parkinson's disease (PD). Pharmacology of the 7 herbs and their major relative polyphenols is depicted in the article .http://www.ncbi.nlm.nih.gov/pubmed/22070681
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Post by beebs on May 11, 2012 15:42:24 GMT -5
This study shows that oxygen deprived cells and glucose starved cells swell by >34 % and that cells, and mitochondrial membrane of the glial cells (look it up, not difficult to understand), worsened. This could lead to head pressures, cognitive dysfunction, intracranial head pressures etc... In contrast, cells that were exposed to cinnamon extract had no swelling!! Glutamate uptake was lessened. The study does not discuss a connection with drug injury, nor do other studies, but Ayurvedic lit does include drug injury as a trigger!! As a side note, the study does not mention Ayurvedic medicine, it was conducted in the USA by the Dept of Agriculture. A procyanidin type A trimer from cinnamon extract attenuates glial cell swelling and the reduction in glutamate uptake following ischemia-like injury in vitro.Panickar KS, Polansky MM, Graves DJ, Urban JF Jr, Anderson RA. Source United States Department of Agriculture, Agricultural Research Service, Beltsville Human Nutrition Research Center, Diet, Genomics and Immunology Laboratory, Beltsville, MD 20705, USA. kiran.panickar@ars.usda.gov Abstract Dietary polyphenols exert neuroprotective effects in ischemic injury. The protective effects of a procyanidin type A trimer (trimer 1) isolated from a water soluble cinnamon extract (CE) were investigated on key features of ischemic injury, including cell swelling, increased free radical production, increased intracellular calcium ([Ca(2+)](i)), mitochondrial dysfunction, and the reduction in glutamate uptake. Astrocyte (glial) swelling is a major component of cytotoxic brain edema in ischemia and, along with vasogenic edema, may contribute to increased intracranial pressure, brain herniation, and additional ischemic injuries. C6 glial cultures were exposed to oxygen-glucose deprivation (OGD) for 5 h, and cell swelling was determined at 90 min after the end of OGD. OGD-induced increases in glial swelling were significantly blocked by trimer 1, but not by the major nonpolyphenol fractions of CE including cinnamaldehyde and coumarin. Increased free radical production, a contributing factor in cell swelling following ischemic injury, was also significantly reduced by trimer 1. Mitochondrial dysfunction, another key feature of ischemic injury, is hypothesized to contribute to glial swelling. Depolarization of the inner mitochondrial membrane potential (ΔΨ(m)) was assessed using a fluorescent dye (tetramethylrhodamine ethyl ester [TMRE]), and was significantly attenuated by trimer 1 as was OGD-induced increased [Ca(2+)](i). Taken together with our previous observation that blockers of [Ca(2+)](i) reduce cell swelling, our results indicate that trimer 1 may attenuate cell swelling by regulating [Ca(2+)](i). Trimer 1 also significantly attenuated the OGD-induced decrease in glutamate uptake. In addition, cyclosporin A, a blocker of the mitochondrial permeability pore (mPT), but not FK506 (that does not block the mPT), reduced the OGD-induced decline in glutamate uptake indicating a role of the mPT in such effects. Thus, the effects of trimer 1 in attenuating the reduction in glutamate uptake are likely mediated through their action on the mitochondria. www.ncbi.nlm.nih.gov/pubmed/22166344
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