5 replies to this topic

[zen]

The article http://www.guardian....-ageing-process describes a link between NF-kB and aging in mice. I did a quick search and found http://jsnn.ncat.unc...oposal-seminar/ which suggest that there might be a connection between C60 and NF-kB. What is your take on this?

[AdamI]

It's interesting that they find that hypothalamus in the brain Controls aging. Then I Guess more People will start taking Epithalon/AGAG now then, since that is the Place where AGAG is produced...? http://www.ncbi.nlm....pubmed/18383712

[AdamI]

maybe I was wrong about what I just wrote...

[AdamI]

"possible mechanism of interaction with NF-KB and ROS" We do know that C60 enters the cell soo it affects ROS mostlikely, maybe NF-KB activation is a response to the Level of ROS, soo C60 doesn't actualy interact with NF-KB, just an effect of the lower ROS that causes NF-KB regulation? What happens to NF-KB if one manage up "regulate" ROS?

[hav]

The article http://www.guardian....-ageing-process describes a link between NF-kB and aging in mice. I did a quick search and found http://jsnn.ncat.unc...oposal-seminar/ which suggest that there might be a connection between C60 and NF-kB. What is your take on this?

The first article finds that suppressing NF-kB and increasing GnRH makes mice live longer:

Further work showed that NF-kB lowered levels of a hormone called GnRH, which is better known for the central role it plays in fertility and the development of sperm and eggs. When the scientists gave old mice daily jabs of GnRH, they found this too extended the animals' lives, and even caused fresh neurons to grow in their brains.

If I understand the 2nd article, it suggests that ROS attacks the NF-kB signal pathway in a way that activates it which promotes a number of diseases, presumably also with a decrease in GnRH, a process that c60 prevents:

Nuclear factor kappa B (NF-kB) is one critical protein that may be targeted by ROS, where the activation of the NF-kB signal transduction pathway (a set of protein reactions that activate NF-kB) by ROS is involved with pathological disorders such as inflammatory diseases, rheumatoid arthritis and lung diseases.

Here's another study about how a GnRH agonist, Triptorelin, has a curative effect that can be obtained by activating NF-kB and thereby lowering GnRH:

Gonadotropin-releasing hormone receptor-targeted gene therapy of gynecologic cancers (also see: full-text)

GnRH Agonist Triptorelin-Induced NFκB Activation In vivo
...
In summary, the proof-of-principle of the GnRH-R-targeted gene therapy could be shown in vitro and in vivo on tumor-bearing nude mice. The tumor volume in mice receiving gene therapy was significantly lower compared with control animals. Toxic side effects were not observed.

Triptorelin is apparently used as a prostate, breast, and ovarian cancer treatment. But if you consider it as a longevity supplement, it is not without side-effects. Same for GnRH agonists generally.

Howard

Edited by hav, 06 May 2013 - 04:00 PM.

[HighDesertWizard]

There are a good number of studies which highlight the role of NF-kb in the aging process. NF-kb inhibition is toward the top of my list of things to try to do. Here's a study reinforcing that importance that I came across just this morning...

 

Motif module map reveals enforcement of aging by continual NF-κB activity

 

Aging is characterized by specific alterations in gene expression, but their underlying mechanisms and functional consequences are not well understood. Here we develop a systematic approach to identify combinatorial cis-regulatory motifs that drive age-dependent gene expression across different tissues and organisms. Integrated analysis of 365 microarrays spanning nine tissue types predicted fourteen motifs as major regulators of age-dependent gene expression in human and mouse. The motif most strongly associated with aging was that of the transcription factor NF-κB. Inducible genetic blockade of NF-κB for 2 wk in the epidermis of chronologically aged mice reverted the tissue characteristics and global gene expression programs to those of young mice. Age-specific NF-κB blockade and orthogonal cell cycle interventions revealed that NF-κB controls cell cycle exit and gene expression signature of aging in parallel but not sequential pathways. These results identify a conserved network of regulatory pathways underlying mammalian aging and show that NF-κB is continually required to enforce many features of aging in a tissue-specific manner.

 

PDF link here.

Edited by wccaguy, 02 November 2014 - 11:23 PM.