NF-?B Inhibition Extends Life in Flies

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squeegee

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NF-?B is associated with a range of interesting mechanisms: "Aging is associated with NF-?B-dependent pro-inflammation. Here we demonstrated that inhibition of NF-?B with pyrrolidine dithiocarbamate increases the median lifespan (13-20%) and the age of 90% mortality (11-14%) in Drosophila melanogaster females and males, respectively. ... NF-?B controls the expression of genes involved in innate immunity, inflammation and apoptosis. Such age-dependent pathologies as tissue inflammation and atrophy are caused by over-activation of the NF-?B signaling with age. ... Recent studies suggest that the NF-?B transcription factor controls age-dependent changes in inflammation genes expression. Donato et al showed that an increase of NF-?B dependent genes in human endothelium with age is primarily linked to [decreased] NF-?B inhibition. Age-associated expression of NF-?B-dependent genes cause progression of atherosclerosis in rat. Furthermore, selective inhibition of NF-?B activity in blood vessel endothelial cells prevents atherosclerosis progression. Genetic blockade of NF-?B in the skin of chronologically aged mice reverses the global gene expression program and tissue characteristics to those of young mice ... However, the effect of NF-?B inhibition on the lifespan was not studied before."

Merely this example "Genetic blockade of NF-?B in the skin of chronologically aged mice reverses the global gene expression program and tissue characteristics to those of young mice" is a very very interesting and possibly a significant "clue"... Certain genes start "drifting" from the optimal state due to lack of pressure from a natural selection, a cellular mess begins, you restore some of that to it's former state - voila, tissue goes back to "young". That's a great proof of the regulation of gene expression relation to the "aging state" of a tissue, and quite probably - a whole organism (I'm not educated enough to speculate how possible it would be to affect a whole epigenome of a mice and "bring it back" to the one it was when a mice was young, if that's possible at all, but I'd bet that would translate in the same effect - overall "age reversal".)..
Key words - "Gene expression program".
 
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http://www.ncbi.nlm.nih.gov/pubmed/15955209

Sulfasalazine inhibits activation of nuclear factor-kappaB in patients with ulcerative colitis.
Gan hair transplant, Chen YQ, Ouyang Q.
Source

Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu, China. ganhuatian@hotmail.com
Abstract
BACKGROUND:

Although sulfasalazine is widely used to treat inflammatory bowel disease, its mechanisms of action remain unclear. Activation of transcription factor nuclear factor (NF)-kappaB, which controls transcription of various pro-inflammatory cytokine genes, has been shown to play a critical role in the pathogenesis of inflammatory bowel disease. The purpose of the present study was to determine whether sulfasalazine therapy affected NF-kappaB activation and the expression of pro-inflammatory cytokines in patients with ulcerative colitis.
METHODS:

A total of 38 patients with moderate ulcerative colitis were investigated. Twenty-one patients received sulfasalazine. Seventeen patients did not receive any medication. Biopsy specimens were obtained from inflamed mucosa and analyzed for NF-kappaB DNA binding activity, NF-kappaBp65/IkappaBalpha protein expression and the levels of pro-inflammatory cytokine mRNA using electrophoretic mobility shift assay, western blot analysis, immunohistochemical staining and reverse transcription-polymerase chain reaction (RT-PCR) analysis, respectively.
RESULTS:

Increased activation of NF-kappaB and high levels of the expression of interleukin (IL)-1beta mRNA and IL-8 mRNA were detected in biopsy specimens from patients with ulcerative colitis. Therapeutic administration of sulfasalazine effectively downregulated the activation of NF-kappaB and the expression of IL-1beta mRNA and IL-8 mRNA while IkappaBalpha levels were stable.
CONCLUSION:

The therapeutic benefits for ulcerative colitis of sulfasalazine might at least in part be attributed to its ability to inhibit NF-kappaB activation, resulting in the downregulation of pro-inflammatory cytokine mRNA expression.

This is maybe why people on Sulfasalazine grow all their hair back with Sulfasalazine.
 
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http://webcache.googleusercontent.com/s ... ogle.co.uk

squee u got some mad good ideas bruv.... i love reading the studies you post

Im very interested in this NF-kB sh*t , i belive inflamination caused by dht is the cause of hairloss not the dht itself

NF-?B Inhibition + spermidine + keratin + minoxidil + L-Arganine + Taurine

i think those in topical form would work way better then any other hairloss topical on the market, mabey some copper peptides thrown in for effect

Edit: Plus this option is non hormonal.... messing with DHT, testosterone and oestrogen on a systematic level is dangerous in my own personal opinion.

I think DHT was a desperate attempt which has blossomed into one of the biggest lies in hairloss.

man + DHT = No hair Loss
man + DHT = hair Loss
man + Low DHT = No hair Loss
man + low DHT = Hair Loss
man + High DHT = No hair Loss
man + High DHT = Hair loss

the above proves this... Also, im a natural bodybuilder, but i know alot of people who juice and ive been a member on bodybuilding.com for years

When you take oral or injectable harsh steroids, Your testosterone and DHT levels sky rocket into the 1000% increase mark. How come some men have no hair loss after abusing steroids for literally decades...

You cant just say " oh its the number of androgen receptors on your head " or " some people are more sensitive to DHT then others " ... come on now, were not idiots here are we ?
 
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