Androgens Damage Hair Via Ros-mediated Tgf-beta, Prevented By Nac

whatevr

whatevr

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Induction of transforming growth factor-beta 1 by androgen is mediated by reactive oxygen species in hair follicle dermal papilla cells

The progression of androgenetic alopecia is closely related to androgen-inducible transforming growth factor (TGF)-β1 secretion by hair follicle dermal papilla cells (DPCs) in bald scalp. Physiological levels of androgen exposure were reported to increase reactive oxygen species (ROS) generation. In this study, rat vibrissae dermal papilla cells (DP-6) transfected with androgen receptor showed increased ROS production following androgen treatment. We confirmed that TGF-β1 secretion is increased by androgen treatment in DP-6, whereas androgeninducible TGF-β1 was significantly suppressed by the ROSscavenger, N-acetyl cysteine. Therefore, we suggest that induction of TGF-β1 by androgen is mediated by ROS in hair follicle DPCs.

TL;DR:
  • Androgens upregulate TGF-beta via reactive oxygen species
  • TGF-beta inhibits hair proliferation and sends follicles into catagen (shedding)
  • Antioxidant N-Acetyl-Cysteine prevented the androgen induced secretion of TGF-beta in dermal papilla cells

Also related:

TGF-beta seems to promote the synthesis of DKK2:
Elevated DKK2 levels could be explained by elevated transforming growth factor β1 (TGF-β1) in OA osteoblasts, and exogenous TGF-β1 increased DKK2 expression in normal osteoblasts, whereas ablating TGF-β1 expression in OA osteoblasts reduced DKK2 expression.
(source: https://www.ncbi.nlm.nih.gov/pubmed/21312269)

DKK2 rather significantly negatively affects hair growth and may potentially be implicated in baldness:
https://www.hairlosscure2020.com/category/dkk2/
 
BetaBoy

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Interesting, I take N-Acetyl-Cysteine (NAC) to help treat a hair related BFRB I struggle with, AFAIK the pathway it targets is unrelated to how this study suggests it may help treat ΑGΑ. Things to know about NAC is that it has a pretty poor half life, I have to take a dose every 4 hours if I want to maintain it's effectiveness throughout the day.
 
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Tommybommy1363

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I’ve been taking NAC for almost 5 months now. Been taking propecia and rogaine same amount of time though
 
whatevr

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Xander94

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I have always been a big advocate of nac time to megadose again
 
ZenHead

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Interesting, since i am using minoxidil i might try to extract and dissolve some NAC into my minoxidil. Any thoughts on this?
 
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Ayr9

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One can take curcumin..It reduces tgf beta 1 at multiple sites of the body
 
Lurker85

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I took 600mg of NAC orally for about 6 months with no significant gains to report.
 
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Otis Mack

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NAC-amide is what we want but I dont know if is available?

https://www.ncbi.nlm.nih.gov/pubmed/23472882



N-Acetylcysteine amide: a derivative to fulfill the promises of N-Acetylcysteine.
Sunitha K1, Hemshekhar M, Thushara RM, Santhosh MS, Yariswamy M, Kemparaju K, Girish KS.
Author information
1
DOS in Biochemistry, University of Mysore, Manasagangothri, Mysore, India.
Abstract
In the present human health scenario, implication of oxidative stress in numerous pathologies including neurodegenerative, cardiovascular, liver, renal, pulmonary disorders, and cancer has gained attention.

N-Acetylcysteine (NAC), a popular thiol antioxidant, has been clinically used to treat various pathophysiological disorders. However, NAC therapy is routine only in paracetamol intoxication and as a mucolytic agent.


Over six decades, numerous studies involving NAC therapy have yielded inconsistent results, and this could be due to low bioavailability. In order to overcome the limitations of NAC,


an amide derivative N-Acetylcysteine amide (NACA) has been synthesized to improve the lipophilicity, membrane permeability, and antioxidant property.

Recent studies have demonstrated the blood-brain barrier permeability and therapeutic potentials of NACA in neurological disorders including Parkinson's disease, Alzheimer's disease, Multiple sclerosis, Tardive dyskinesia, and HIV-associated neurological disorders.

In addition, NACA displays protective effect against pulmonary inflammation and antibiotic-induced apoptosis.

Forthcoming research on the possible therapeutic properties of NACA and its generics in the management of pathologies associated with extracellular matrix degradation and oxidative stress-related inflammation is highly exciting.


Superior bioavailability of NACA is likely to fulfill the promises of NAC as well as a molecule to improve the endurance and resident time of bioscaffolds and biomaterials. Till date, more than 800 reviews on NAC have been published. However, no comprehensive review is available on the therapeutic applications of NACA. Therefore, the current review would be the first to emphasize the therapeutic potentials of NACA and its derivatives.
 
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