linl1: Acta Pharmacol Sin. 2004 Jul;25(7):869-75.Links
Effects of sodium beta-aescin on expression of adhesion molecules and migration of neutrophils after middle cerebral artery occlusion in rats.Hu XM, Zhang Y, Zeng FD.
Institute of Clinical Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, China.
AIM: To investigate the effects of sodium beta-aescin on neutrophil migration and expression of adhesion molecules (ICAM-1 and E-selectin) after middle cerebral artery occlusion (MCAO) in rats. METHODS: Rats were pretreated with sodium beta-aescin for 7 d and then subjected to cerebral ischemia/reperfusion (I/R) injury induced by an MCAO. After a 2-h ischemia and a 24-h reperfusion, the infarct volume and neurological deficit were determined by the method of TTC staining and the Longa's score. The effect of sodium beta-aescin on the migration of neutrophils was evaluated by measuring the activity of myeloperoxidase (MPO) enzyme. The expressions of adhesion molecules were determined by immunohistochemistry and Western blot. RESULTS: Sodium beta-aescin significantly reduced the cerebral infarct volume and ameliorated the neurological deficit (P<0.05 or P<0.01). The MPO activity and the expressions of ICAM-1 and E-selectin in the vehicle-treated rats were increased significantly (P<0.01) after cerebral I/R. After treatment with sodium beta-aescin, the enzymatic activity of MPO and the expressions of these adhesion molecules were significantly reduced compared with the vehicle-treated group (P<0.05 or P<0.01). CONCLUSION: Sodium beta-aescin can attenuate brain injury, down-regulate the protein expressions of ICAM-1 and E-selectin, and reduce the migration of neutrophils after cerebral I/R.
PMID: 15210059 [PubMed - indexed for MEDLINE]
link1: Neurosci Lett. 2008 Oct 24;444(2):195-8. Epub 2008 Aug 15. Links
Elevated myeloperoxidase activity in white matter in multiple sclerosis.Gray E, Thomas TL, Betmouni S, Scolding N, Love S.
MS Laboratories, Burden Centre, University of Bristol Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1JB, United Kingdom.
Recent studies have revealed extensive axonal damage in patients with progressive multiple sclerosis (MS). Axonal damage can be caused by a plethora of factors including the release of proteolytic enzymes and cytotoxic oxidants by activated immune cells and glia within the lesion. Macrophages and microglia are known to express myeloperoxidase (MPO) and generate reactive oxygen species during myelin phagocytosis in the white matter. In the present study we have measured MPO levels in post-mortem homogenates of demyelinated and non-demyelinated regions of white matter from nine patients with MS and seven controls, and assessed MPO immunoreactivity within MS brain. In homogenates of MS white matter, demyelination was associated with significantly elevated MPO activity when compared to controls. Immunohistochemistry showed MPO to be expressed mainly by macrophages within and adjacent to plaques. Demyelination in MS is associated with increased activity of MPO, suggesting that this production of reactive oxygen species may contribute to axonal injury within plaques.
PMID: 18723077 [PubMed - in process]
link1: Free Radic Biol Med. 2008 Sep 1;45(5):726-31. Epub 2008 Jun 3. Links
Microglia and myeloperoxidase: a deadly partnership in neurodegenerative disease.Lefkowitz DL, Lefkowitz SS.
School of Biological Sciences, Section of Molecular Genetics and Microbiology, University of Texas at Austin, 1 University Station A5000, Austin, TX 78712-0162, USA. firstname.lastname@example.org
The role of inflammation in Alzheimer's disease, Parkinson's disease, and multiple sclerosis has recently come under increased scrutiny. Associated with these inflammatory responses are tumor necrosis factor-alpha (TNF-alpha) and reactive oxygen species (ROS), both believed to be derived from brain microglia. In addition to the above, the presence of myeloperoxidase (MPO) in these diseased brains has been reported by a number of investigators. However, the possible role of MPO and enzymatically inactive MPO (iMPO) as the "choreographers" of the destruction done by TNF-alpha and ROS is not generally recognized. Previously, our laboratory has reported that MPO/iMPO enhance macrophage generation of ROS and expression of proinflammatory cytokine genes as well as gene products. Recent studies in our laboratory indicate that the same response occurs with microglia. A paradigm is presented for the perpetuation of inflammation associated with neurodegenerative diseases. This model describes the unrecognized consequences of the stimulation of microglia by MPO or iMPO. Both MPO and iMPO and/or its receptor may represent new therapeutic targets for the treatment of these diseases.
PMID: 18554520 [PubMed - indexed for MEDLINE]
link1: Brain. 2008 Apr;131(Pt 4):1123-33. Epub 2008 Jan 29. Links
Myeloperoxidase-targeted imaging of active inflammatory lesions in murine experimental autoimmune encephalomyelitis.Chen JW, Breckwoldt MO, Aikawa E, Chiang G, Weissleder R.
Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, 5404 Building 149, 13th Street, Charlestown, MA 02129, USA. email@example.com
Inflammatory demyelinating plaques are the pathologic hallmark of active multiple sclerosis and often precede clinical manifestations. Non-invasive early detection of active plaques would thus be crucial in establishing pre-symptomatic diagnosis and could lead to early preventive treatment strategies. Using murine experimental autoimmune encephalomyelitis as a model of multiple sclerosis, we demonstrate that a prototype paramagnetic myeloperoxidase (MPO) sensor can detect and confirm more, smaller, and earlier active inflammatory lesions in living mice by in vivo MRI. We show that MPO expression corresponded with areas of inflammatory cell infiltration and demyelination, and higher MPO activity as detected by MPO imaging, biochemical assays, and histopathological analyses correlated with increased clinical disease severity. Our findings present a potential new translational approach for specific non-invasive inflammatory plaque imaging. This approach could be used in longitudinal studies to identify active demyelinating plaques as well as to more accurately track disease course following treatment in clinical trials.
PMID: 18234693 [PubMed - indexed for MEDLINE]
link1: Int Angiol. 1999 Dec;18(4):306-12.Links
Effect of Ruscus extract and hesperidin methylchalcone on hypoxia-induced activation of endothelial cells.Bouaziz N, Michiels C, Janssens D, Berna N, Eliaers F, Panconi E, Remacle J.
Laboratoire de Biochimie et Biologie Cellulaire--Facultés Universitaires Notre-Dame de la Paix--Namur, Belgium.
BACKGROUND: Ruscus aculeatus extract and the flavonoid hesperidin methylchalcone (HMC) are drugs used in the treatment of chronic venous insufficiency. METHODS: In the present study, we investigated their effects on the activation of endothelial cells by hypoxia, a condition which mimics venous blood stasis. RESULTS: We observed that Ruscus extract was able to inhibit the activation of endothelial cells by hypoxia: the decrease in ATP content, the activation of phospholipase A2 as well as the subsequent increase in neutrophil adherence with a maximal protection obtained at 50 microg/ml. HMC was also able to inhibit the hypoxia-induced decrease in ATP content. Furthermore, the effects of Ruscus extract and of HMC on this decrease seem to be additive. CONCLUSIONS: The biochemical mechanism evidenced in this work might explain some of the beneficial therapeutic effects of these products in the treatment of chronic venous insufficiency patients.
PMID: 10811519 [PubMed - indexed for MEDLINE]
link1: J Pharmacol Sci. 2008 Oct;108(2):198-205. Links
Possible Mechanism of the Anti-inflammatory Activity of Ruscogenin: Role of Intercellular Adhesion Molecule-1 and Nuclear Factor-kappaB.Huang YL, Kou JP, Ma L, Song JX, Yu BY.
Department of Complex Prescription of TCM, China Pharmaceutical University, China.
Ruscogenin (RUS), first isolated from Ruscus aculeatus, also a major steroidal sapogenin of traditional Chinese herb Radix Ophiopogon japonicus, has been found to exert significant anti-inflammatory and anti-thrombotic activities. Our previous studies suggested that ruscogenin remarkably inhibited adhesion of leukocytes to a human umbilical vein endothelial cell line (ECV304) injured by tumor necrosis factor-alpha (TNF-alpha) in a concentration-dependent manner. Yet the underlying mechanisms remain unclear. In this study, the in vivo effects of ruscogenin on leukocyte migration and celiac prostaglandin E(2) (PGE(2)) level induced by zymosan A were studied in mice. Furthermore, the effects of ruscogenin on TNF-alpha-induced intercellular adhesion molecule-1 (ICAM-1) expression and nuclear factor-kappaB (NF-kappaB) activation were also investigated under consideration of their key roles in leukocyte recruitment. The results showed that ruscogenin significantly suppressed zymosan A-evoked peritoneal total leukocyte migration in mice in a dose-dependent manner, while it had no obvious effect on PGE(2) content in peritoneal exudant. Ruscogenin also inhibited TNF-alpha-induced over expression of ICAM-1 both at the mRNA and protein levels and suppressed NF-kappaB activation considerably by decreasing NF-kappaB p65 translocation and DNA binding activity. These findings provide some new insights that may explain the possible molecular mechanism of ruscogenin and Radix Ophiopogon japonicus for the inhibition of endothelial responses to cytokines during inflammatory and vascular disorders.
PMID: 18946195 [PubMed - in process]
1: J Neurol Neurosurg Psychiatry. 2003 Jul;74(7):953-5. Links
Low leucocyte myeloperoxidase activity in patients with multiple sclerosis.Ramsaransing G, Teelken A, Prokopenko VM, Arutjunyan AV, De Keyser J.
Department of Neurology, Academisch Ziekenhuis Groningen, Groningen, Netherlands.
The gene for myeloperoxidase (MPO) has been implicated in multiple sclerosis (MS). By measuring H(2)O(2) dependent oxidation of 3,3'5,5'-tetramethylbenzidine with spectrophotometry the authors investigated MPO activity in peripheral blood leucocytes from 42 patients with MS (12 with secondary progressive MS, 17 with primary progressive MS, and 13 with relapsing remitting benign MS) and 32 healthy controls. Leucocyte MPO activity was significantly lower in patients with benign MS (mean (SEM) 0.086 (0.029) U/mg protein; p<0.01), secondary progressive MS (0.038 (0.009) U/mg protein; p<0.001), and primary progressive MS (0.057 (0.016) U/mg protein; p<0.001) compared with healthy controls (0.322 (0.053) U/mg protein). These data suggest that low MPO, which may be genetically determined, plays a part in MS pathogenesis.
PMID: 12810789 [PubMed - indexed for MEDLINE]
1: J Neuroimmunol. 2001 Jan 1;112(1-2):97-105. Links
Mice lacking myeloperoxidase are more susceptible to experimental autoimmune encephalomyelitis.Brennan M, Gaur A, Pahuja A, Lusis AJ, Reynolds WF.
Departments of Medicine, Microbiology and Molecular Genetics and Human Genetics, UCLA, 47-123 Center for Health Sciences, Los Angeles, CA 90095, USA.
EAE is a demyelinating disease which serves as an animal model for multiple sclerosis (MS). Myeloperoxidase (MPO) has been implicated in MS through its presence in invading macrophages, and by association of a -463G/A promoter polymorphism with increased risk. Also, MPO at 17q23.1 is within a region identified in genome scans as a MS susceptibility locus. We here examine the incidence of EAE in MPO knockout (KO) mice. MPO is detected in invading macrophages in the CNS of wild-type mice, yet unexpectedly, MPO-KO mice have significantly increased incidence of EAE: Ninety percent of MPO-KO mice developed complete hind limb paralysis as compared to 33% of wildtype (WT) littermates (P<0.0001). This is the first evidence that MPO plays a significant role in EAE, consistent with its postulated role in MS.
PMID: 11108938 [PubMed - indexed for MEDLINE]
link1: J Neuroimmunol. 1997 Sep;78(1-2):97-107. Links
Immunohistochemical and genetic evidence of myeloperoxidase involvement in multiple sclerosis.Nagra RM, Becher B, Tourtellotte WW, Antel JP, Gold D, Paladino T, Smith RA, Nelson JR, Reynolds WF.
Neurology Research Service, West Los Angeles VA Medical Center and Brain Research Institute, CA 90073, USA.
The myeloperoxidase enzyme (MPO) is expressed specifically in myeloid cells and catalyzes the formation of hypochlorous acid and other cytotoxic oxidants. We previously reported that two alleles of MPO exist which differ in promoter strength due to a base difference in an Alu-encoded hormone response element. The present study shows that the higher expressing MPO genotype is overrepresented in early onset multiple sclerosis in females, implicating MPO in this demyelinating disease. Contrary to the general conception that macrophages lack MPO, immunohistochemical analysis shows that MPO is present in microglia/macrophages in and around MS lesions as shown by colocalization with major histocompatibility antigens HLA-DR and phagocytized myelin. Also, MPO mRNA sequences are detected in cDNA derived from isolated human adult microglia. This is the first evidence that MPO is present in microglia/macrophages at MS lesions, that MPO gene expression occurs in microglia and that MPO plays a role in MS pathogenesis as shown by the allelic disequilibrium in early onset disease.
PMID: 9307233 [PubMed - indexed for MEDLINE]
Is that a dare? huh?gibbledygook wrote:which are much more conservative than when I first started. I can't believe how much ginkgo I started with! I currently take somewhat more than you on a daily basis
Thats almost nothinggibbledygook wrote: and 4.8g of salvia.
I am about 67kg and 5foot 10 (...and a bit...), so that means (using dosage per kg) I would need to take just under 20% more than you.gibbledygook wrote:I weigh about 57kg to 60kg and am 5foot 7 inches. Maybe weight and height are also factors...
Sure, the old "do as I say, not as I do"gibbledygook wrote:Not a dare! No way. I think it's much better going slowly (although that is not what I ever seem to do).
I slowly (ie over 3 days for both Salvia and Ginkgo) built to the dosages I mentioned, just in case I had any negative effect.gibbledygook wrote:Actually, looking at your dose of salvia it seems odd that you're not noticing anything... Yes, it was 10grams of salvia alone that was the dosage that had such an impressive effect on me....But go slowly!!
Thoughts; your MS may be more based around a damaged BBB? the ginkgo I use is supposedly the one they used in one of the trials, and so may have less of the negative chemical in it, and it may be this chemical that you actually reacted badly to, not the ginkgo. I don't know either.gibbledygook wrote:But then you are a bit heavier. I'm perplexed.
OK, you win!gibbledygook wrote:Don't do what I do and neck a bottle just to see what happens!!!!!
This is the Salvia i purchased from iHerb. It is not red either. In real life I think I can see a very slight tinge of dark green.gibbledygook wrote:I just saw my Chinese doctor who told me that salvia has a distinct red appearance. My salvia from herbalextractsplus is distinctly green. Is it in fact salvia?! I shall switch to the brand available from iherb tomorrow and see what happens then.
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