This is topic What can help inactivate NFkB - review in forum Medical Questions at LymeNet Flash.


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Posted by Marnie (Member # 773) on :
 
Although it was not known until 1998 that

ibuprofen inhibited NFKB,

knowledge of that fact is not required under existing patent law principles of inherency. It is enough that the drug inhibited NFKB.

Other well known drugs that also inhibit NFKB include aspirin , the immunosuppressive drug gliotoxin , and

the rheumatoid arthritis treatment

***sulfasalazine.*** Hummmm.
http://www.rheumatology.org/public/factsheets/sulfasalazine.asp

NFKB inhibitors that people have used for thousands of years include garlic, red wine, capsaicin (the "hot" ingredient in peppers), and caffeic acid (from honeybee propolis, the material used to seal the honeycomb). Even vitamin E inhibits NFKB.

http://www.pharmexec.com/pharmexec/article/articleDetail.jsp?id=53001

Here is a list of things that can impact NFkB:

curcumin

magnesium (but Bb has a Mg transporter gene

lipoic acid (upregulated in lyme via Omega 6s)

vitamin E (gamma E?)

Black Raspberry Extracts

zinc (Bb has "zinc fingers"...depleting our zinc levels.

glutathione (deficient in lyme because it needs cysteine - to be made and cysteine is a component of zinc fingers)

Far infrared saunas

Oscillations (like the Soloflex machine).

Why oscillations?

J Biol Chem. 2001 Apr 20;276(16):13499-504. Epub 2000 Nov 28.

Oscillating fluid flow inhibits TNF-alpha -induced NF-kappa B activation via an Ikappa B kinase pathway in osteoblast-like UMR106 cells.

Kurokouchi K, Jacobs CR, Donahue HJ.
Department of Orthopaedics and Rehabilitation and Cellular and Molecular Physiology, Musculoskeletal Research Laboratory, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.

luid flow plays an important role in load-induced bone remodeling.

However, the molecular mechanism of flow-induced signal transduction in osteoblasts remains unclear.

In endothelial cells, fluid flow alters activation of NF-kappaB resulting in changes in expression of cell adhesion molecules.

To test the hypothesis that fluid flow alters NF-kappaB activation and expression of cell adhesion molecules in osteoblastic cells,

we examined the effect of oscillating fluid flow (OFF) on tumor necrosis factor (TNF)-alpha-induced NF-kappaB activation in rat osteoblast-like UMR106 cells.

We found that OFF inhibits NF-kappaB-DNA binding activities, especially TNF-alpha-induced p50-p65 heterodimer NF-kappaB activation and TNF-alpha-induced intercellular adhesion molecule-1 mRNA expression.

The inhibitory effects of OFF on both TNF-alpha-induced NF-kappaB activation and intercellular adhesion molecule-1 mRNA expression were shear stress-dependent and also increased with OFF exposure duration, indicating that OFF has potent effects on mechanotransduction pathways.

OFF also inhibited TNF-alpha-induced IkappaBalpha degradation and TNF-alpha-induced IkappaB kinase (IKK) activity in a shear stress-dependent manner.

These results demonstrate that IKK is an initial target molecule for OFF effects on osteoblastic cells.

Thus, OFF inhibits TNF-alpha-induced IKK activation, leading to a decrease in phosphorylation and degradation of inhibitory IkappaBalpha, which in turn results in the decrease of TNF-alpha-induced NF-kappaB activation and potentially the transcription of target genes.

PMID: 11096064
 


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