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"sertaconazole treatment resulted in the activation of p38 MAP kinase and its downstream substrate, the small heat-shock protein 27 (Hsp27), in a dose- and time-dependent manner. "
I made thread about heatshockproteins potentially helping hair growth here, if someone has a bit more data on it...!
Next, we evaluated the effect of different concentrations of sertaconazole on PGE2 production from HaCaT keratinocytes. Figure 2b shows that sertaconazole treatment results in a twofold increase in PGE2 release. To assess the involvement of COX-2 in sertaconazole-mediated PGE2 release, cells were preincubated with NS398, a specific inhibitor of COX-2 (Gierse et al., 1995) before sertaconazole treatment. Sertaconazole-mediated PGE2 production was inhibited in the presence of the COX-2 inhibitor (Figure 2b), suggesting the involvement of COX-2 in PGE2 production. Next, we evaluated whether sertaconazole regulated the TNF-α-dependent PGE2 production in these cells and interestingly it was observed that in a similar manner sertaconazole upregulated TNF-α-induced PGE2 release (Figure 2c)."
www.sciencedirect.com/science/article/pii/S0022202X15337428
It has been shown in multple studies that tnf-a is actually important in the early phase of the wounding process for hair follicle neogenesis. Maybe this is directliy connected to pge2? Last wounding session I used 4.5 hours before diclofenac as NSAIDs did show to increase TNF-A. If so, this might be even better with wounding than that. (you find everything regarding tnf-a wounding by search function or also linked in my fractional laser wounding thread )
Now, I found setaconazole also mentions in swisstemples ask.fm, he answered that he answered the question already, I cannot find it though... So, I am not sure what is the issue with it as pge2 agonist could be, considering has not been listed as pge2 agonist.
Edit: Seems to increase pgd2 also. I thought about that before, anyways, it is similiar to minoxidil then. Can be tried but should be used at least with an antiandrogen or even better: a pgd2 inhibitor.
The p38 MAP kinase is activated in response to various extracellular stimuli such as UV light, heat, osmotic shock, inflammatory cytokines, and growth factors (Zarubin and Han, 2005).
Thus, from these results, we believe that sertaconazole stimulates superoxide radical formation to induce p38 MAP kinase
Sertaconazole did not increase H2O2 formation in human keratinocytes (data not shown) and treatment with catalase was ineffective in reducing the phosphorylation of p38 by sertaconazole, suggesting that the peroxide formation was not a factor in p38 activation. In contrast to sertaconazole, another antifungal agent, miconazole nitrate, was shown to induce H2O2 formation (Kobayashi et al., 2002); however, miconazole does not inhibit cytokine release or elicit anti-inflammatory activity comparable with sertaconazole (Agut et al., 1996; Liebel et al., 2006) and therefore does not probably activate the same signal transduction cascade. Thus, from these results, we believe that sertaconazole stimulates superoxide radical formation to induce p38 MAP kinase
Miconazole was shown to be PGE1. Someone here actually had some success with it (inspired by Brotzu), and swiss was/is also using it.
PGE1 and PGE2 are both known to be positively for our hair, nonetheless they have an antagonistic character to each other. For minoxidil it is for example argued that it increases pge1 and pge2 (if you are responder), however because of this effect you apparently end up with more pge1. Im not part of that private forum, so I am not 100% yet what makes them believe that pge1 wins the battle here.
Anyways, you see here two exact oppositve mechanisms, pge2 is considered to be stronger as it turns into pgf2a and its four recepter seem to have different kind of benefits. Ep3 for example turns into fgf9 for example, which was shown to be missing on the wounding process of humans, multiple productlines seem to be incoming in future based on this finding. ( 1 , 2 ) It makes perfectly sense, one being PGE1 and PGE2 or at least it would not be surprising at all...
I wrote already more than I wanted. I think it is worth trying, especially with wounding due to increased tnf-a-pge2 induction. If someone tries it, pls do a picture protocoll (you dont need to show your face ofc! No need to feel unconfortable).
Thanks for the read. I hope this gets some attention.
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