mrhodes40 wrote:The simple idea that MS might be something like a germ appears to potentially be fraught with all of these complicated co factors that require far more of your doctor that 'an antibiotics prescription'. Since this may be true, it may be a long time before all the ins and outs are understood and a genuinely, repeatably successful regimen is clearly illucidated.
meantime these are interesting discussions!
Tissue plasminogen activator (abbreviated tPA or PLAT) is a protein involved in the breakdown of blood clots.
Plasminogen activator inhibitor-1 is the principal inhibitor of tissue plasminogen activator (tPA) and urokinase (uPA), the activators of plasminogen and hence fibrinolysis (the physiological breakdown of blood clots).
<shortened url>1: J Cell Biochem. 2005 Sep 1;96(1):109-16. Links
Salvianolic acid B attenuates plasminogen activator inhibitor type 1 production in TNF-alpha treated human umbilical vein endothelial cells.Zhou Z, Liu Y, Miao AD, Wang SQ.
Beijing Institute of Radiation Medicine, Beijing, 100850, People's Republic of China.
Plasminogen activator inhibitor type 1 (PAI-1), which plays a role in the development of atherosclerosis, is produced by endothelial cells following stimulation with various inflammatory cytokines such as tumor necrosis factor (TNF-alpha). In the present study, we investigated the effects of a potent water-soluble antioxidant, salvianolic acid B (SalB; derived from the Chinese herb, Salvia miltiorrhiza), on the expression of PAI-1 in TNF-alpha-treated human umbilical vein endothelial cells (HUVECs). We found that SalB inhibited TNF-alpha-induced PAI-1 mRNA production and protein secretion in HUVECs. Treatment with SalB (0.05 and 0.15 microM) notably attenuated TNF-alpha induced expression of PAI-1 to 90.5% and 74.6%, respectively, after 12 h, and to 75.1% and 64.2%, respectively, after 18 h. We also observed a dose-dependent decrease in PAI-1 protein production in the presence of SalB. We then used pathway inhibitors to investigate which step of the TNF-alpha induced signaling pathway was targeted by SalB. We found that the c-Jun N-terminal kinase (JNK) inhibitor, SP600125, increased the inhibitory effects of SalB on TNF-alpha-induced PAI-1 secretion, whereas the nuclear factor-kappaB (NF-kappaB) inhibitor, emodin, and the extracellular signal-regulated kinase (ERK) inhibitor, PD98059, did not. A gel shift assay further showed that SalB inhibited the TNF-alpha-activated NF-kappaB and AP-1 DNA binding activities in a dose-dependent manner. Collectively, these results indicate that the NF-kappaB and ERK-AP-1 pathways are possible targets of SalB in the regulation of TNF-alpha-stimulated PAI-1 production in HUVECs. Copyright 2005 Wiley-Liss, Inc
PMID: 16052513 [PubMed - indexed for MEDLINE]
...serum levels of vitamin E and the serum vitamin E/cholesterol ratio were significantly lower in MS patients when compared with controls...
...tricky though, because if blood is making it through the BBB and is leaking into the brain, you would think you'd want it thicker if anything...
The major forms of vitamin E in human physiological fluids are alpha and gamma tocopherols which exhibit different biological activities under a variety of assay conditions... processes involved in the entry of tocopherol from blood to the CSF do not discriminate between the alpha and gamma tocopherols. In contrast, alpha tocopherol is highly preferred during the packaging of plasma lipoproteins by the liver. Our data also suggest that alpha and gamma tocopherols will be available to the human brain via transport from blood.
The natural vitamin E tocotrienol (TCT) possesses biological properties not shared by tocopherols (TCP). Nanomolar alpha-TCT, not alpha-TCP, is potently neuroprotective... Orally supplemented alpha-TCT was delivered to all vital organs including the brain and spinal cord in significant amounts... alpha-TCT accumulated in vital organs over more than 2 years was almost completely lost in less than 2 months when the supplementation was stopped. This is in sharp contrast with findings related to alpha-TCP retention. The ability of long-term oral supplementation to maintain and elevate alpha-TCT levels in vital organs together with the rapid elimination of the intact vitamin from all organs studied underscores the need for continuous oral supplementation of TCT.
...Tocotrienol-treated primary neurons maintained healthy growth and motility even in the presence of excess glutamate...
gamma-tocotrienol was the most cardioprotective of all the isomers. This is an interesting finding with far reaching consequence as the gamma-tocotrienol form (including gamma-tocopherol) is the most abundantly found in our diet
...The therapeutic dosage is high, between about 800 mg to about 10 grams of gamma-tocopherol and between about 50 mg to about 5 grams of gamma-tocotrienol per day.
rainer wrote:Here is another article on this topic. A little easier to read then the last one I posted, and has some nice diagrams.
Fibrin Mechanisms and Functions in Nervous System Pathology
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