Modified citrus pectin

If it's on your mind and it has to do with multiple sclerosis in any way, post it here.

Modified citrus pectin

Postby Anonymoose » Wed Nov 21, 2012 8:23 am

I am following the Wheldon protocol and have found that mcp helps immensely with the resulting inflammation. I've done a little research on mcp and suspect that it's ability to bind to inflammation causing galectin-3 (present in elevated levels in ms and arteriosclerosis plaques) is what makes it so helpful to me. It also acts as a gentle chelator. It might be of use to pwms even if they aren't on an antibiotic protocol so I thought I'd share.
Anonymoose
Family Elder
 
Posts: 1024
Joined: Tue Oct 09, 2012 7:33 am

Re: Modified citrus pectin

Postby Anonymoose » Wed Nov 21, 2012 8:25 pm

Or it could help because of this...

10Chen CH, Sheu MT, Chen TF, Wang YC, et al. Suppression of endotoxin-induced proinflammatory responses by citrus pectin through blocking LPS signaling pathways. Biochemical Pharmacology, 2006;72(8):1001-1009.

Purpose: Mechanism for reduction of inflammation response
Type of Animal: BALB/c mice and macrophage cell line RAW264.7
Type of Cancer: All types (reduction of inflammation process)
Experiment Description:
Methods: Experimental mouse and macrophage cells were plated and pre-treated with three types of citrus pectins ( DE30, DE60 and DE90) and LPS (lipopolysaccharide from Escherichia coli 0127:B8) for six to 24 hours followed by a series of molecular assays (i.e., western blot analysis, RT-PCR, LPS binding) on the cells. A second set of experiments focused on DE90 pectin and the expression of iNOS (nitric oxide synthase) and COX-2 (cyclooxygenase-2) protein expression triggered by LPS.
Results: iNOS and COX-2 expression and mRNA expression were significantly inhibited by the three types of pectin (p<0.01). DE90 was the pectin that most strongly inhibited these proteins (p<0.01). Further results indicated downregulation of iNOS and COX-2 protein expression.
Anonymoose
Family Elder
 
Posts: 1024
Joined: Tue Oct 09, 2012 7:33 am

Inos and ms. Mcp suppresses inos production...

Postby Anonymoose » Thu Nov 22, 2012 7:30 am

Inducible nitric oxide synthase in chronic active multiple sclerosis plaques: distribution, cellular expression and association with myelin damage.

AuthorsHill KE, et al. Show all Journal
J Neuroimmunol. 2004 Jun;151(1-2):171-9.
Affiliation
Neurovirology Research Laboratory Veterans Affairs SLCHCS, and Department of Neurology, University of Utah, Salt Lake City, USA.
Abstract
Inducible nitric oxide synthase (iNOS) is an enzyme that produces nitric oxide (NO) and is thought to contribute to the pathogenesis of multiple sclerosis (MS). The extent of iNOS expression was examined using laser scanning confocal microscopy of 13 chronic active plaques from seven MS patients displaying both acute demyelination and active inflammation. iNOS expression in these plaques was substantial and diverse in cellular distribution. Expression of iNOS was observed in ependymal cells located in periventricular lesions, inflammatory cells, and occasionally in astrocytes. iNOS was found in microglial/macrophage cells that expressed CD64, the high affinity Fc gamma receptor associated with cells that have phagocytic function and participate in antibody-dependent cellular cytotoxicity (ADCC). Scavenger microglial/macrophage cells that expressed the marker CD14 were also present and may express iNOS. The markers for myelin damage, nitrotyrosine (an index of iNOS mediated damage via peroxynitrite formation), along with MBP fragments, were also observed associated with iNOS in MS plaques. Together, these findings support a central role for iNOS in the pathogenesis of multiple sclerosis.

PMID 15145615 [PubMed - indexed for MEDLINE]
Full text: Elsevier Science
Anonymoose
Family Elder
 
Posts: 1024
Joined: Tue Oct 09, 2012 7:33 am

Re: Modified citrus pectin

Postby Anonymoose » Thu Nov 22, 2012 7:45 am

Cox2 and myelin damage. Mcp inhibits cox2 expression.

CONCLUSIONS: COX-2 expression was associated with dying oligodendrocytes in MS lesions and appeared to increase excitotoxic death of oligodendrocytes in culture. An understanding of how COX-2 expression influences oligodendrocyte death leading to demyelination may have important ramifications for future treatments for MS.


http://www.ncbi.nlm.nih.gov/m/pubmed/20 ... 63/related
Anonymoose
Family Elder
 
Posts: 1024
Joined: Tue Oct 09, 2012 7:33 am

Or it could help because it inhibits IL-6...

Postby Anonymoose » Thu Nov 22, 2012 11:29 am

However, the side effects of spironolactone are significant while MCP is proven to achieve greater results without toxicity or side effects. Specifically, the MCP was shown to outperform spironolactone in a few key areas related to inflammation and fibrosis. MCP achieved better suppression of fibrotic markers. Importantly, MCP completely inhibited the cytokine interleukin-6 (IL-6) which plays a key role in inflammation, fibrosis, immune response and cancer/metastasis.  Spironolactone only partially blocked the Aldo induced IL-6.

http://www.bizjournals.com/sacramento/p ... 20/AQ15591


IL6 in ms and transverse myelitis 
http://www.sciencedirect.com/science/ar ... 0X96002833

http://onlinelibrary.wiley.com/store/10 ... fd7a802dc4

http://www.xagena.it/news/medicinenews_ ... 0fb61.html
Anonymoose
Family Elder
 
Posts: 1024
Joined: Tue Oct 09, 2012 7:33 am

Re: Modified citrus pectin

Postby Anonymoose » Mon Nov 26, 2012 11:33 am

Possible CCSVI connection....could Aldo induced fibrosis cause initial vein narrowing and re-stenosis after treatment? If so, it seems MCP may help on that horizon as well. Binding Galectin-3 would limit Aldo induced vascular fibrosis...

Aldosterone and vascular damage
Daniel Duprez MD, DSc, PhD, Marc De Buyzere BSc, Ernst R. Rietzschel MD, Denis L. Clement MD, PhD
Look Inside Get Access
Abstract
Although the aldosterone escape mechanism is well known, aldosterone has often been neglected in the pathophysiologic consequences of the activated renin-angiotensinaldosterone system in arterial hypertension and chronic heart failure. There is now evidence for vascular synthesis of aldosterone aside from its secretion by the adrenal cortex. Moreover, aldosterone is involved in vascular smooth muscle cell hypertrophy and hyperplasia, as well as in vascular matrix impairment and endothelial dysfunction. The mechanisms of action of aldosterone may be either delayed (genomic) or rapid (nongenomic). Deleterious effects of aldosterone leading to vascular target-organ damage include (besides salt and water retention) decreased arterial and venous compliance, increased peripheral vascular resistance, and impaired autonomic vascular control due to baroreflex dysfunction.

http://link.springer.com/article/10.100 ... -z?LI=true


Galectin-3 Mediates Aldosterone-Induced Vascular Fibrosis.
Laurent C, Maria M, Pascal R, Victoria C, Ernesto MM, de Boer RA, Françoise P, Patrick L, Faiez Z, Patrick R, Natalia LA.
Source
INSERM.
Abstract
OBJECTIVE:
Aldosterone (Aldo) is involved in arterial stiffness and heart failure, but the mechanisms have remained unclear. Galectin-3 (Gal-3), a β-galactoside-binding lectin, plays an important role in inflammation, fibrosis, and heart failure. We investigated here whether Gal-3 is involved in Aldo-induced vascular fibrosis.
METHODS AND RESULTS:
In rat vascular smooth muscle cells Gal-3 overexpression enhanced specifically collagen type I synthesis. Moreover Gal-3 inhibition by modified citrus pectin or small interfering RNA blocked Aldo-induced collagen type I synthesis. Rats were treated with Aldo-salt combined with spironolactone or modified citrus pectin for 3 weeks. Hypertensive Aldo-treated rats presented vascular hypertrophy, inflammation, fibrosis, and increased aortic Gal-3 expression. Spironolactone or modified citrus pectin treatment reversed all the above effects. Wild-type and Gal-3 knock-out mice were treated with Aldo for 6 hours or 3 weeks. Aldo increased aortic Gal-3 expression, inflammation, and collagen type I in wild-type mice at both the short- and the long-term, whereas no changes occurred in Gal-3 knock-out mice.
CONCLUSIONS:
Our data indicate that Gal-3 is required for inflammatory and fibrotic responses to Aldo in vascular smooth muscle cells in vitro and in vivo, suggesting a key role for Gal-3 in vascular fibrosis.
PMID: 23117656 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/23117656
Anonymoose
Family Elder
 
Posts: 1024
Joined: Tue Oct 09, 2012 7:33 am

A Patent for treatment of neurodegenerative disease w/ MCP

Postby Anonymoose » Wed Nov 28, 2012 11:31 am

United States Patent Application 20060014719
Kind Code A1
Chang; Yan January 19, 2006

--------------------------------------------------------------------------------
Method for treating neurodegenerative diseases


Abstract
The present invention is directed to methods and compositions for treatment of neurodegenerative diseases. In particular embodiments, the invention is directed to the treatment of Alzheimer's disease, MS, ALS, Huntington's Disease. In other embodiments, the invention is directed to the treatment of multiple sclerosis.



0017] Cell adhesion and activation of endothelial cell walls are important components of diseases such as MS or AD. The process involves a complex cascade of various molecules and mediators, including chemokines, adhesion molecules, and matrix metalloproteases. One important set of components is integrins, which may mediate the progression of these diseases.

[0018] Integrins are the principal receptors on animal cells for binding most extracellular matrix proteins, including collagen, fibronectin, and laminin. Integrins form a large family of homologous transmembrane linker proteins, and are the main way that cells bind to and respond to the extracellular matrix. Integrins are heterodimers of .alpha. and .beta. subunits, and the ligand-binding site is composed of parts of both chains. In mammals, at least 22 integrin heterodimers, composed of 17 types of .alpha. subunits and 8 types of .beta. subunits, are known. A single .beta. chain can interact with multiple a chains, forming integrins that bind different ligands.

[0019] .beta. integrins are generally believed to be directly associated with focal adhesion kinase (FAK). Constitutive activation of FAK is sufficient to rescue epithelial cells from anoikis, whereas apoptosis occurs if FAK is inhibited by, for example, a peptide representing the FAK-binding site of .beta.1 integrin. Several proteins that lie downstream to .beta.1 integrin in this signal transduction pathway have been identified, two of which are Akt and PI-3 kinase. Akt is a survival-promoting Ser-Thr protein kinase whose activity is regulated by a variety of growth factors in a PI 3-kinase-dependent manner. Activation of Akt has been shown to result in inhibition of apoptosis in several types of cells, including primary culture of cerebellar neurons, Rat-1, and COS-7 cells. P13 kinase and Akt both can be direct or indirect down stream effectors of FAK.

[0020] There is evidence that the carbohydrate polymer for the use in the method of present invention interacts directly or indirectly with integrins, more specifically .beta. integrins, and prevents or attenuates the progression of the inflammatory neurodegenerative diseases. The carbohydrate useful to carry out the methods of the present invention has been shown to downregulate both FAK and Akt.


The carbohydrate polymer is modified citrus pectin. Yadda yadda yadda more at...

http://appft1.uspto.gov/netacgi/nph-Par ... 0060014719
Anonymoose
Family Elder
 
Posts: 1024
Joined: Tue Oct 09, 2012 7:33 am

Re: Modified citrus pectin

Postby Anonymoose » Wed Nov 28, 2012 12:25 pm

Angiogenesis in multiplesclerosis: is it good, bad or an epiphenomenon?
Shauna Kirka,
Joseph A. Frankb,
Stephen Karlik
http://www.sciencedirect.com/science/ar ... 0X03003368
Image
Fig. 1. Potential role for angiogenesis in MS. (1) Initially immune cells bind to the BBB through a variety of cell adhesion molecules. (2) Cells infiltrate the perivascular space. (3) Cytokine, immune and antibody mediated attack on the myelin in the perivascular space. (4) Infiltration of immune cells into the parenchyma. (5) Release of inflammatory and hypoxic mediators including VEGF, HIF-1, NO, ET-1 from various cell types. (6) Angiogenic signals cause the initiation of the formation of new blood vessels into the lesion area.


http://journals.lww.com/jneuropath/Abst ... _in.9.aspx
Vascular Endothelial Growth Factor Is Expressed in Multiple Sclerosis Plaques and Can Induce Inflammatory Lesions in Experimental Allergic Encephalomyelitis Rats


PROESCHOLDT, MARTIN A. MD; JACOBSON, STEVEN PHD; TRESSER, NANCY MD; OLDFIELD, EDWARD H. MD; MERRILL, MARSHA J. PHD

Abstract

The active lesions in multiple sclerosis (MS) are characterized by blood-brain-barrier (BBB) breakdown, upregulation of adhesion molecules on capillary endothelial cells, and perivascular inflammation, suggesting that altered vessel permeability and activated endothelial cells are involved in the pathogenesis of the disease. Vascular endothelial growth factor (VEGF) mediates multiple aspects of blood vessel physiology, including regulation of growth, permeability, and inflammation. To investigate a possible relationship between VEGF expression and CNS autoimmune disease, we examined VEGF expression in MS plaques compared to normal white matter by immunohistochemistry and in situ hybridization. VEGF expression was consistently upregulated in both acute and chronic MS plaques. We also examined VEGF expression during the course of experimental allergic encephalomyelitis (EAE) in rats. VEGF-positive cells with astrocytic morphology increased in the spinal cord during the development of EAE and were found in association with inflammatory cells. Furthermore, intracerebral infusion of VEGF in animals previously immunized with myelin basic protein induced an inflammatory response in the brain, whereas infusion of vehicle, or infusion of VEGF in naive animals, did not. These results suggest that overexpression of VEGF may exacerbate the inflammatory response in autoimmune diseases of the CNS by inducing focal BBB breakdown and migration of inflammatory cells into the lesions.


And another Yan Chang Patent claiming MCP controls angiogenesis
http://patft1.uspto.gov/netacgi/nph-Par ... PN/6890906

The present invention recognizes the role of galectins in angiogenesis, and provides a therapeutic material which will advantageously interact with galectins so as to moderate or prevent the manifestations of angiogenesis-dependent disease. Specifically, the present invention recognizes that particular carbohydrate materials will bind to or otherwise interact with galectins and thereby modify their interaction with cellular structures, and thereby control angiogenesis.

Galectins comprise a family of proteins which are expressed by plant and animal cells, and which bind .beta.-galactoside sugars. These proteins can be found on cell surfaces, in cytoplasm, and in extracellular fluids. They have a molecular weight in the general range of 29-34 kd; they have an affinity for .beta.-galactoside containing materials, and have been found to play important roles in a number of biological processes. Galectin-1 and galectin-3 are specific members of this family which have been found to interact with various cellular structures, and galectin-3 has been demonstrated to promote angiogenesis in vitro.



Yadda yadda yadda including a chart (more legible in google patents) showing lab results of the impact of MCP on VEGF levels (it decreased VEGF significantly)
Anonymoose
Family Elder
 
Posts: 1024
Joined: Tue Oct 09, 2012 7:33 am

Re: Modified citrus pectin

Postby baja655 » Wed Jul 30, 2014 3:23 pm

I am soooo happy to find this site today and hear successes and research on mcp. I have sclerosis in my jaws and scarring in my lungs and plaque in the carotid arteries but yet to be formally diagnosed. I stumbled on pectin after finding cough drops that had pectin in them instead of menthol. I got curious as to why pectin in the cough drops so I started researching on pectin and found the research on binding and helping remove plaque. I would love any success anyone has had with pectin.
baja655
Newbie
 
Posts: 1
Joined: Wed Jul 30, 2014 3:19 pm


Return to General Discussion

 


  • Related topics
    Replies
    Views
    Last post

Who is online

Users browsing this forum: No registered users


Contact us | Terms of Service