Could someone interpret the last two sentences please.
Based on the rest of the article it appears to be saying in fibroblasts (they don’t know if this is true of every human cell type) that Minocycline repairs the metabolic activity that was stopped by finastride, a potent 5ar type II inhibitor and continues the conversion from testosterone to DHT and other substrates.
basically they are saying that that:
- For periosteal fibroblasts coming from oral periosteum isolated from the bone surface
- And regarding Testosterone conversion into DHT, through 5AR2
Mynocicline increases the synthesis of DHT
Finasteride decreases it, with a statistically insignificant change in 17beta-hydroxysteroid dehydrogenase activity (I think this is important).
I think they may be suspecting that in case there is a need for adjuntive treatment with Monocycline, because there is a metabolic activity at that diseased tissue, and that metabolic activity is not desired, it’s better to block it with a 5ar2 like finasteride?
May be that I got it all wrong…but i think there’s nothing very helpful here with exception that:
- monocycline does the exact opposite of finasteride
- finasteride doesn’t induce a significant change in 17beta-hydroxysteroid dehydrogenase
here:
ncbi.nlm.nih.gov/pubmed/9477022
"Abstract
In addition to their antimicrobial properties, tetracyclines have antiinflammatory and pro-anabolic effects on the reparatory potential of connective tissue and bone. The physiologically active androgen 5alpha-dihydrotestosterone (DHT) implicated in matrix synthesis is formed in gingivae from androgen substrates. The aim of this investigation is to study the androgen metabolic response of gingivae to minocycline, in the presence or absence of the anti-androgen finasteride. Chronically inflamed gingival tissue derived from 12 subjects aged 30-50 years and passaged fibroblasts derived from this source, were used for the experiments. Duplicate incubations were performed in Eagle’s MEM with 14C-testosterone/14C-4-androstenedione in the presence or absence of minocycline (5-60 microg/ml) or finasteride for 24 h. The androgen substrate 14C-testosterone was metabolised mainly to DHT and 4-androstenedione, while 14C-4-androstenedione was converted mainly to DHT and testosterone. Minocycline at 20-30 microg/ml stimulated the formation of these metabolites from both substrates by 13-25%. In the tissue incubations there were 3- and 2-fold increases in DHT and 4-androstenedione formation (n=12; p<0.01). The anti-androgen finasteride caused significant inhibition of 5alpha-reductase activity on both substrates at 0.1 & 1.0 microg/ml with total inhibition at 10 & 50 microg/ml (n=3; p<0.01). Minocycline-induced stimulation of 5alpha-reductase activity was also inhibited by finasteride (n=4; p<0.02). Since finasteride inhibition of 5alpha-reductase activity is specific for the type 2 isoenzyme associated with anabolic functions of target tissue, this enzyme activity may contribute to some of the cited anabolic tissue responses to minocycline."
Basically they are trying to identify who’s responsible for the anabolic responses of these tissues, and they used a 5AR2 inhibitor to understand if it’s 5AR2 the responsible…and it is.
this mean monocycline increases 5AR2 activity!
Thanks, Mew actually posted this a few years ago but I wasn’t 100% clear on its implications.
Strange how its used as anti-acne treatment given that it stimulates DHT synthesis.
funny…could be that it’s got different actions in different tissues…and possibly at different dosages.
could be useful for gyno!
I seem to recall some people used minocycline here with mixed results…