Newly Discovered Factor in Androgenetic Alopecia. The Cure is Near?

2020

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After castration your Cox levels are going down ......this is why. Prostaglandins are products of COX. Higher Cox= unprugulated prostagladins. finasteride works for a reason:)

then how come castrated people don't regrow all of their hair back?

how come PGD2 stays there and keeps inhibiting follicle growth?
bald2.jpg



IS IT POSSIBLE, that the same "prostaglandin profile" exists near follicles that are in TELOGEN phase?
 

squeegee

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Inflammation and ROS already damaged the area..Inhibition of hair growth =Apoptosis
 

Boldy

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Maybe this sounds crazy, But I have the feeling that the inhibition has something to do with Oxygen..

Im investigating the link between oxygen and PGE2 and other hormones.
 

zombiehair

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onions contain quercetin which suppresses pgd2 from reading the below text it sounds like onions may also have pge-like activity.
win win ?
thoughts.
Allium species (onion and garlic) which are known as folk medicine for the treatment of atherosclerosis and some ulcers, were shown to be rich in two trihydroxylated derivatives of 18:2(n-6) : 9,10,13- and 9,12,13-trihydroxy octadecenoic acids. Furthermore, it was shown that these products have PGE-like activity in in vitro bio-assay tests (Claeys M et al., Prog Lipid Res 1986, 25, 53). Similar products were isolated from roots of Bryone ala, used also for similar medicinal purposes as onion (Panossian AG et al., J Med Plant Res 1983, 47, 17).
 

zombiehair

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here we go :)
Prostaglandins. 1985 May;29(5):847-65.

Isolation and identification of two isomeric trihydroxy octadecenoic acids with prostaglandin E-like activity from onion bulbs (Allium cepa).

Ustünes L, Claeys M, Laekeman G, Herman AG, Vlietinck AJ, Ozer A.


Abstract

Two fractions with prostaglandin E-like activity were isolated from onion (Allium cepa) by using XAD-2 adsorption, silicic acid column chromatography and thin layer chromatography. The fractions were analyzed by gas chromatography/mass spectrometry and were characterized as isomeric mixtures of 9,10,13-trihydroxy-11-octadecenoic and 9,12,13-trihydroxy-10-octadecenoic acid, which are lipoxygenase metabolites of linoleic acid. Bio-assay, for which cascade superfusion was used and the rabbit coeliac and mesenteric arteries and the rat fundus strip were employed as assay organs, was utilized to monitor the bio-active profile throughout the isolation procedures. The activity of 1 microgram of the pharmacologically active fractions T1 and T2 was found to be equivalent to that of respectively 1.33 and 0.63 ng of prostaglandin E2.

those ancients with their traditional cures might not have been to far off target.
to me it looks like onions will suppress pgd2 and mimic pge2 ,is this not what we are looking for :)
 

2020

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Inflammation and ROS already damaged the area..Inhibition of hair growth =Apoptosis

that actually may be good news since Histogen may actually be able to reverse that and repopulate follicles with missing cells. As long as there isn't some switch that permanently changes cycle functioning, we should be good.


about my first point:
IS IT POSSIBLE, that excess PGD2 in bald scalp IS EXPECTED due to all hairs there being in RESTING PHASE? In which case, blocking PGD2 would only prolong the hair cycles a bit but still wouldn't prevent the inevitable just like minoxidil/latisse....

- - - Updated - - -

Maybe this sounds crazy, But I have the feeling that the inhibition has something to do with Oxygen..

Im investigating the link between oxygen and PGE2 and other hormones.

are you saying that because of that new discovery from Loreal?
 

odalbak

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"In that model we showed that PGD2 started to go up during the end of the growing phase and was highest at catagen, the stage of regression. " Cotzarelis

From what I read here and there Prostaglandins often have antagonist effects. For instance PGF2 promotes bronchoconstriction whereas PGE2 promotes bronchodilatation. Is there the same antagonism in Androgenetic Alopecia, with PGE2 enabling hair growth during the growth phase and PGD2 enabling hair regression during the regression phase?
 

Saint-Loup

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Inflammation and ROS already damaged the area..Inhibition of hair growth =Apoptosis
PGD2 and its main metabolite 15d-PGJ2 seem to generate or enhance ROS in some kinds of cells.

The cytotoxicity of 15d-PGJ2 was associated with the production of ROS and was inversely related to intracellular glutathione (GSH) levels. However, the cytotoxicity of 15d-PGJ2 was not decreased by the free radical scavengers ascorbic acid or α-tocopherol.
15d-PGJ2 induces apoptosis of mouse oligodendrocyte precursor cells
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1941731/
 

Saint-Loup

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But NAC seems to be able to counteract this effect.

15d-PGJ(2) was also found to induce Reactive Oxygen Species generation and partially blocked nuclear factor-kappaB activity. Pretreatment with antioxidant N-acetylcysteine prevented the p53 accumulation, the phosphorylations of JNK and p38 MAPK, the inhibition of NF-kappaB activity, as well as the apoptosis induced by 15d-PGJ(2). Using a mouse model of corneal neovascularization, it was demonstrated in vivo that 15d-PGJ(2) induced Reactive Oxygen Species generation, activated JNK and p38 MAPK, induced p53 accumulation/phosphorylation, and induced vascular endothelial cell apoptosis, which could be abolished by N-acetylcysteine, SP600125, SB203580, or a virus-derived amphipathic peptides-based p53 small interfering RNA.

15-deoxy-Delta(12,14)-prostaglandin J2 induces vascular endothelial cell apoptosis through the sequential activation of MAPKS and p53
http://www.ncbi.nlm.nih.gov/pubmed/18718914
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The cyclopentenone prostaglandin 15-deoxy-delta 12,14-prostaglandin J2 (15d-PGJ2) induces apoptosis in various cell types.
JNK activation by 15d-PGJ2 was blocked by antioxidants N-acetylcysteine (NAC) and GSH. 15d-PGJ2 caused ROS generation and 15d-PGJ2-induced cell death was prevented by antioxidants, suggesting involvement of ROS generation in 15d-PGJ2-induced cell death.15d-PGJ2 triggered the mitochondrial apoptotic pathway indicated by enhanced Bax expression, loss of mitochondrial membrane potential, cytochrome c release, and caspase-3 activation.

15-Deoxy-delta 12,14-prostaglandin J2 induces apoptosis via JNK-mediated mitochondrial pathway in osteoblastic cells
http://www.ncbi.nlm.nih.gov/pubmed/18450357
 

Saint-Loup

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are you saying that because of that new discovery from Loreal?
Hello 2020
Your signature is no longer visible.
I remember it was dealing with a useful Proxy software or website.
Could you send me the URL of this website please?
Thank you.

(I will delete this post later sorry but his PMbox is full)
 

squeegee

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Loup buddy!!! awesome work there!!
 

zombiehair

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Nice post on 15d-PGJ2 saint loup.
From what ive read on 15d-PGJ2 since seeing your post it looks like 15d-PGJ2 is the end product of pgd2 so not sure we have to worry about this if we are going to be blocking pgd2 ?
cheers
 

squeegee

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cox as c****.. 2020..
 

Quadzilla99

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But NAC seems to be able to counteract this effect.


15d-PGJ(2) was also found to induce Reactive Oxygen Species generation and partially blocked nuclear factor-kappaB activity. Pretreatment with antioxidant N-acetylcysteine prevented the p53 accumulation, the phosphorylations of JNK and p38 MAPK, the inhibition of NF-kappaB activity, as well as the apoptosis induced by 15d-PGJ(2). Using a mouse model of corneal neovascularization, it was demonstrated in vivo that 15d-PGJ(2) induced Reactive Oxygen Species generation, activated JNK and p38 MAPK, induced p53 accumulation/phosphorylation, and induced vascular endothelial cell apoptosis, which could be abolished by N-acetylcysteine, SP600125, SB203580, or a virus-derived amphipathic peptides-based p53 small interfering RNA.


15-deoxy-Delta(12,14)-prostaglandin J2 induces vascular endothelial cell apoptosis through the sequential activation of MAPKS and p53
http://www.ncbi.nlm.nih.gov/pubmed/18718914
------


The cyclopentenone prostaglandin 15-deoxy-delta 12,14-prostaglandin J2 (15d-PGJ2) induces apoptosis in various cell types.
JNK activation by 15d-PGJ2 was blocked by antioxidants N-acetylcysteine (NAC) and GSH. 15d-PGJ2 caused ROS generation and 15d-PGJ2-induced cell death was prevented by antioxidants, suggesting involvement of ROS generation in 15d-PGJ2-induced cell death.15d-PGJ2 triggered the mitochondrial apoptotic pathway indicated by enhanced Bax expression, loss of mitochondrial membrane potential, cytochrome c release, and caspase-3 activation.


15-Deoxy-delta 12,14-prostaglandin J2 induces apoptosis via JNK-mediated mitochondrial pathway in osteoblastic cells
http://www.ncbi.nlm.nih.gov/pubmed/18450357
Makes sense. NAC is a precursor to glutathione. There's a thread here about how the skin cells of men with male pattern baldness are glutathione deficient for some reason. Problem is supplementing with NAC to augment glut. is tricky after a while it causes a decrease in glutathione. The most absorbable form of alpha lipoic acid (NA-Rala) is also a potent glutathione precursor.

http://forum.bodybuilding.com/showthread.php?t=111178821&highlight=glutathione


http://forum.bodybuilding.com/showthread.php?t=128976301&highlight=glutathione

dkbDC.png


what are you talking about? Am I wrong?
http://www.urbandictionary.com/define.php?term=cockblocking
 

squeegee

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Every Chronic inflammation related diseases =Low Glutathione ...male pattern baldness is nothing but inflammation. PGD2 are messenger of inflammation and our scalp are flooded of it LOL...
 
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