Can anyone tell me or provide a link explaining what these are? I have a study that suggests they may be beneficial for my type of hair loss, but I can't for the life of me figure out what they are (ie brand names, or even names of chemical/substances). Any help would be very much appreciated.
Topical TFG beta II inhibitor
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Dice_Has_Hair
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TGF-b inhibitors inhibit TGF-b(transforming growth factor) which is involved in the immune systems response to the genetically predisposed hair follicles. It's good for male pattern baldness.chew said:
science-jay
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Dice_Has_Hair said:TNF-a inhibitors inhibit TNF-a(tumor necrosis factor) which is involved in the immune systems response to the genetically predisposed hair follicles. It's good for male pattern baldness.chew said:
That's right Dice, and green tea is a major TNF-alpha as well a TNF-kappa-b blocker!
Green tea epigallocatechin-3-gallate mediates T cellular NF-kappa B inhibition and exerts neuroprotection in autoimmune encephalomyelitis.
Aktas O, Prozorovski T, Smorodchenko A, Savaskan NE, Lauster R, Kloetzel PM, Infante-Duarte C, Brocke S, Zipp F.
Institute of Neuroimmunology, Neuroscience Research Center, Charite, Berlin, Germany.
Recent studies in multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), point to the fact that even in the early phase of inflammation, neuronal pathology plays a pivotal role in the sustained disability of affected individuals. We show that the major green tea constituent, (-)-epigallocatechin-3-gallate (EGCG), dramatically suppresses EAE induced by proteolipid protein 139-151. EGCG reduced clinical severity when given at initiation or after the onset of EAE by both limiting brain inflammation and reducing neuronal damage. In orally treated mice, we found abrogated proliferation and TNF-alpha production of encephalitogenic T cells. In human myelin-specific CD4+ T cells, cell cycle arrest was induced, down-regulating the cyclin-dependent kinase 4. Interference with both T cell growth and effector function was mediated by blockade of the catalytic activities of the 20S/26S proteasome complex, resulting in intracellular accumulation of IkappaB-alpha and subsequent inhibition of NF-kappaB activation. Because its structure implicates additional antioxidative properties, EGCG was capable of protecting against neuronal injury in living brain tissue induced by N-methyl-D-aspartate or TRAIL and of directly blocking the formation of neurotoxic reactive oxygen species in neurons. Thus, a natural green tea constituent may open up a new therapeutic avenue for young disabled adults with inflammatory brain disease by combining, on one hand, anti-inflammatory and, on the other hand, neuroprotective capacities
New TNF-alpha releasing inhibitors as cancer preventive agents from traditional herbal medicine and combination cancer prevention study with EGCG and sulindac or tamoxifen.
Fujiki H, Suganuma M, Kurusu M, Okabe S, Imayoshi Y, Taniguchi S, Yoshida T.
Department of Biochemistry, Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Yamashiro-Cho, Tokushima 770-8514, Japan. hfujiki@ph.bunri-u.ac.jp
Herbal medicines are now attracting attention as potential sources of cancer preventive agents. Using inhibition of tumor necrosis factor-alpha (TNF-alpha) release assay, we studied Acer nikoense, Megusurino-ki in Japanese. Inhibitory potential was found in the leaf extract, and the main active principles were identified as geraniin and corilagin. The IC(50) values for TNF-alpha release inhibition were 43 microM for geraniin and 76 microM for corilagin, whereas that for (-)-epigallocatechin gallate (EGCG), the green tea polyphenol, as control was 26 microM. Furthermore, treatment with geraniin inhibited okadaic acid tumor promotion in a two-stage carcinogenesis experiment on mouse skin. Geraniin and corilagin are present in another well-known Japanese traditional herb, Geranium thunbergii, Genno-shoko in Japanese. Considering seasonal variations of the agents and sites of cultivation of herbs, this paper reviews the significance of geraniin as a new cancer preventive agent. In addition, based on accumulated results of green tea as a cancer preventive, we review two important results with EGCG: the synergistic effects of EGCG with sulindac or tamoxifen on cancer preventive activity in PC-9 cells, and cancer prevention of intestinal tumor development in multiple intestinal neoplasia (Min) mice by cotreatment using EGCG with sulindac. We report here new findings on additional gene expression resulting from cotreatment with EGCG and sulindac in PC-9 cells compared with gene expression by EGCG alone or sulindac alone. Overall, our results indicate that, with the continuing spread of cancer chemoprevention as a fundamental medical strategy, both clinicians and researchers should take a closer look at herbal medicine. Copyright 2002 Elsevier Science B.V.
PMID: 12628509 [PubMed - indexed for MEDLINE]
Dice_Has_Hair
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You should give amashisho a try. All the users that have used it say it works. But, there haven't been many users.luke77 said:
Dice_Has_Hair
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science-jay said:
science-jay
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TNF-A
altough a TNF-alpha inhibitor wouldn't automaticaly stumulate more hair growth:
Etanercept does not effectively treat moderate to severe alopecia areata: an open-label study.
Strober BE, Siu K, Alexis AF, Kim G, Washenik K, Sinha A, Shupack JL.
The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, New York, USA. b_strober@hotmail.com
In this prospective, open-label pilot study, we evaluated the safety and efficacy of etanercept, a TNF-alpha inhibitor, in the treatment of moderate to severe alopecia areata, alopecia totalis, or alopecia universalis. Seventeen otherwise healthy adults with moderate to severe alopecia areata were enrolled. The primary outcome measure was the extent of hair regrowth during and after the end of treatment as evaluated by the Severity of Alopecia Tool (the SALT score). After between 8 and 24 weeks of continuous treatment with etanercept 50 mg given subcutaneously twice weekly, significant regrowth of hair was not shown in any of the subjects treated. Based on these results, etanercept appears to be ineffective in treating subjects with treatment-refractory, moderate to severe alopecia areata, alopecia totalis, or alopecia universalis.
altough a TNF-alpha inhibitor wouldn't automaticaly stumulate more hair growth:
Etanercept does not effectively treat moderate to severe alopecia areata: an open-label study.
Strober BE, Siu K, Alexis AF, Kim G, Washenik K, Sinha A, Shupack JL.
The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, New York, USA. b_strober@hotmail.com
In this prospective, open-label pilot study, we evaluated the safety and efficacy of etanercept, a TNF-alpha inhibitor, in the treatment of moderate to severe alopecia areata, alopecia totalis, or alopecia universalis. Seventeen otherwise healthy adults with moderate to severe alopecia areata were enrolled. The primary outcome measure was the extent of hair regrowth during and after the end of treatment as evaluated by the Severity of Alopecia Tool (the SALT score). After between 8 and 24 weeks of continuous treatment with etanercept 50 mg given subcutaneously twice weekly, significant regrowth of hair was not shown in any of the subjects treated. Based on these results, etanercept appears to be ineffective in treating subjects with treatment-refractory, moderate to severe alopecia areata, alopecia totalis, or alopecia universalis.
Dice_Has_Hair
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Re: TNF-A
Okay, but they didn't mention whether or not it "stopped" the hairloss. The actual stopping of hairloss would be the most realistic thing, right? There are also other things involved in this immune system response than TNF-a. I believe TGF-b and PKC are too.science-jay said:
science-jay
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Re: TNF-A
Dice_Has_Hair said:
Wow, thanks for the resposes so far guys. The reason I was asking for this type of compound is because I suspect that my hairloss was induced by the use of accutane. According to this study, these compounds may be helpful in retinol-induced hair loss. I will look into the amashisho - can anyone that has tried it provide any kind of testimonial? Also, regarding the green tea - I have just started taking gte orally - would it be helpful to apply it topically as well? And how would I go about making a solution - would it dissolve in minoxidil? Thanks again and I will keep you guys up to date with any results. Here's the study:
Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans retinoic acid induces premature hair follicle regression (catagen) by upregulation of transforming growth factor-beta2 in the dermal papilla.
Foitzik K, Spexard T, Nakamura M, Halsner U, Paus R.
Department of Dermatology, University Hospital Hamburg-Eppendorf, University of Hamburg, Hamburg, Germany.
Diffuse hair loss ranks among the most frequent and psychologically most distressing adverse effects of systemic therapy with retinoids, which severely limits their therapeutic use even where clinically desired. Since the underlying mechanisms of retinoid-induced effluvium are as yet unknown, we have investigated the influence of the prototypic retinoid all-trans retinoic acid (ATRA, tretinoin) on the growth of human scalp hair follicles (HF) in culture. HF in the anagen VI stage of the hair cycle were cultured in the presence of 10(-8) or 10(-10) M ATRA. Compared with controls, hair shaft elongation declined significantly already after 2 d in the ATRA-treated group, and approximately 80% of the ATRA-treated HF had prematurely entered catagen-like stage at day 6, compared with 30% in the control group. This corresponded to an upregulation of apoptotic and a downregulation of Ki67-positive cells in ATRA-treated HF. Since transforming growth factor (TGF)-beta has been implicated as a key inducer of catagen, we next studied whether ATRA treatment had any effect on follicular expression. TGF-beta2 immunoreactivity was detected in the outer root sheath of anagen VI scalp HF. In catagen follicles, TGF-beta2 was also expressed in the regressing epithelial strand. After 4 d of ATRA treatment, TGF-beta2 was significantly upregulated in anagen HF in the dermal papilla (DP) and the dermal sheath, 7, and TGF-beta neutralizing antibody partially abrogated at RA induced hair growth inhibition. Real-time PCR confirmed a significant upregulation of TGF-beta2 transcripts in ATRA-treated hair bulbs. This study is the first to provide direct evidence that ATRA can indeed induce a catagen-like stage in human HF and suggests that this occurs, at least in part, via upregulation of TGF-beta2 in the DP. Therefore, topical TGF-beta2/TGF-beta receptor II antagonists deserve to be explored for the prevention and management of retinoid-induced hair loss.
Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans retinoic acid induces premature hair follicle regression (catagen) by upregulation of transforming growth factor-beta2 in the dermal papilla.
Foitzik K, Spexard T, Nakamura M, Halsner U, Paus R.
Department of Dermatology, University Hospital Hamburg-Eppendorf, University of Hamburg, Hamburg, Germany.
Diffuse hair loss ranks among the most frequent and psychologically most distressing adverse effects of systemic therapy with retinoids, which severely limits their therapeutic use even where clinically desired. Since the underlying mechanisms of retinoid-induced effluvium are as yet unknown, we have investigated the influence of the prototypic retinoid all-trans retinoic acid (ATRA, tretinoin) on the growth of human scalp hair follicles (HF) in culture. HF in the anagen VI stage of the hair cycle were cultured in the presence of 10(-8) or 10(-10) M ATRA. Compared with controls, hair shaft elongation declined significantly already after 2 d in the ATRA-treated group, and approximately 80% of the ATRA-treated HF had prematurely entered catagen-like stage at day 6, compared with 30% in the control group. This corresponded to an upregulation of apoptotic and a downregulation of Ki67-positive cells in ATRA-treated HF. Since transforming growth factor (TGF)-beta has been implicated as a key inducer of catagen, we next studied whether ATRA treatment had any effect on follicular expression. TGF-beta2 immunoreactivity was detected in the outer root sheath of anagen VI scalp HF. In catagen follicles, TGF-beta2 was also expressed in the regressing epithelial strand. After 4 d of ATRA treatment, TGF-beta2 was significantly upregulated in anagen HF in the dermal papilla (DP) and the dermal sheath, 7, and TGF-beta neutralizing antibody partially abrogated at RA induced hair growth inhibition. Real-time PCR confirmed a significant upregulation of TGF-beta2 transcripts in ATRA-treated hair bulbs. This study is the first to provide direct evidence that ATRA can indeed induce a catagen-like stage in human HF and suggests that this occurs, at least in part, via upregulation of TGF-beta2 in the DP. Therefore, topical TGF-beta2/TGF-beta receptor II antagonists deserve to be explored for the prevention and management of retinoid-induced hair loss.
Dice_Has_Hair
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I have heard about the accutane doing that to hair. Its a shame. I believe that I read that on http://www.hairsite.com Are you sure that you can't get on another good acne treatment? You should talk to a dermatologist and see if he can suggest you another good treatment that won't affect your hair. Also, to add, accutane is very hard on the liver from what I hear. The liver is something you DEFINITELY do not want to mess with. The healthier your liver is, the longer and healthier you'll live.luke77 said:
As for amashisho usage, I think the only person on this site that has used it was bluesmiley. You might want to do a search. PM him for some info. I am going to give amashisho a try. I have heard good things about it. Nothing bad.
You can buy green tea extract topical solution on http://www.lipoxidil.com I would think that applying it topically would help better for hair than drinking, but drinking is good for overall health.
:wink:
Dice_Has_Hair
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If amashisho is going to do anything, it'll probably stop the hairloss, but as far as regrowing , its questionable. I really think you should drop the accutane and try something else. Hell even folligen would probably help ya with the hairloss.1derphull said:
No, I've been off accutane for a few years, so I am not sure that the accutane caused it. However, the hair loss began soon after my accutane treatment (at a very young age). The only reason I suspect that it may be accutane-induced is because I also experienced some of the other side effects that the "anti-accutane" people complain of - ie abnormal liver function tests, low wbc, etc. Also my hair loss has been diffuse without a whole lot of recession in the front. I'm certainly not saying that accutane definitely caused my hair loss - but it's something to explore, and the "big 3" have not done anything for me except MAYBE slow things down some. Thanks again for the responses so far.
Luke
Luke
Dice_Has_Hair
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You might want to go here > http://www.hairloss-research.org/index.html This site is pretty good. There is a special section called "updates" which you might find especially interesting. The TNF-a, TGF-b, PKC are talked about and inhibiting them as well. I'd read the whole section of updates, its pretty interesting!luke77 said:
:wink: