το εχει ψαξει κανεις η το εχει δοκιμασει,ειμαι ετοιμος να παω να το παραγγειλω θελω να χτυπησω Pgd2 πιο πολυ γιατι το cetrizine την κατεβαζει στο 50% μετα απο 5 ωρες,αν δουλευει καλα το setr πως θα δουλευει αυτο οταν το πιουμε,το καλο ειναι πως βγαινει απο κοκκινο σταφυλι λολ.
Resveratrol internal pgd2 inhibitor
- Έναρξη μίζας cinder
- Ημερομηνία έναρξης
Παρακαλώ συνδεθείτε ή εγγραφείτε για να απενεργοποιήσετε τις διαφημίσεις.
και τοπικα βαζω cetrizine οπως ειχαν πει τα παιδια εδω μεσα, μεχρι στιγμης 1 εβδομαδα αποτελεσματα καθολου φαγουρα πιο δυνατη τριχα.πιστευω πως εσωτερικα ισως να ειναι ακομα καλυτερα αφου βαραει μεσα απο τον οργανισμο την pgd2,στο θεμα αν ειναι ασφαλες το πουλανε χωρις συνταγη και βγαινει οπως ειπα απο κοκκινο σταφυλι οποτε ειναι σχεδον ακακο.γκουγκλαρε το και θα δεις
kapa
Μέλος του προσωπικού
http://www.hairloss-research.org/UpdatePDG7-12.html
Prostaglandin D2 (or PGD2) is a prostaglandin that is central to development of dermatologic inflammation, pattern hair loss, and allergic disorders, such as asthma.
A newly released, 2012 study showed a cause and effect relationship between abnormally high levels of PGD2 and male pattern baldness. With topical application they found PGD2 prevents hair growth, and mice who were genetically predisposed to produce higher levels of PGD2 had diminished hair growth. They additionally discovered PGD2 levels were much elevated in balding scalp versus non-balding scalp tissue. The study concluded that one of the receptors involved in production of PGD2, GPR44, constituted a precise therapeutic target for hormonal hair loss in both men and women.
Sci Transl Med. 2012 Mar 21; 4(126):126ra34.
Prostaglandin D2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia.
Garza LA, Liu Y, Yang Z, Alagesan B, Lawson JA, Norberg SM, Loy DE, Zhao T, Blatt HB, Stanton DC, Carrasco L, Ahluwalia G, Fischer SM, FitzGerald GA, Cotsarelis G.
Source
Department of Dermatology, Kligman Laboratories, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Abstract
Testosterone is necessary for the development of male pattern baldness, known as androgenetic alopecia (AGA); yet, the mechanisms for decreased hair growth in this disorder are unclear. We show that prostaglandin D(2) synthase (PTGDS) is elevated at the mRNA and protein levels in bald scalp compared to haired scalp of men with AGA. The product of PTGDS enzyme activity, prostaglandin D(2) (PGD(2)), is similarly elevated in bald scalp. During normal follicle cycling in mice, Ptgds and PGD(2) levels increase immediately preceding the regression phase, suggesting an inhibitory effect on hair growth. We show that PGD(2) inhibits hair growth in explanted human hair follicles and when applied topically to mice. Hair growth inhibition requires the PGD(2) receptor G protein (heterotrimeric guanine nucleotide)-coupled receptor 44 (GPR44), but not the PGD(2) receptor 1 (PTGDR). Furthermore, we find that a transgenic mouse, K14-Ptgs2, which targets prostaglandin-endoperoxide synthase 2 expression to the skin, demonstrates elevated levels of PGD(2) in the skin and develops alopecia, follicular miniaturization, and sebaceous gland hyperplasia, which are all hallmarks of human AGA. These results define PGD(2) as an inhibitor of hair growth in AGA and suggest the PGD(2)-GPR44 pathway as a potential target for treatment.
Because PGD2's correlation with asthma is well established, several drugs that down regulate PGD2 are already in clinical trials. PGD2 inhibitors would serve to promote hair growth. Scientists involved in this study, including Dr. Cotsarelis of stem cell research renown, state that they’ve already formulated pills containing the vital PGD2 blocking properties. But why wait for an expensive, patented medication. Resveratrol has been shown to significantly suppress PGD2 at low concentrations readily obtainable through oral dosing, as evidenced by the abstract presented below. Oral resveratrol has also been shown to have anti-asthmatic effects superior to that of dexamethasone, the side effect wrought, cortico-steroid of choice for managing asthma symptoms.
Planta Med. 2004 Apr;70(4):305-9.
Resveratrol inhibits the release of mediators from bone marrow-derived mouse mast cells in vitro.
Baolin L, Inami Y, Tanaka H, Inagaki N, Iinuma M, Nagai H.
Source
Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, P. R. China.
Abstract
Resveratrol is a natural phytoalexin occurring in grapes, vines and peanuts and possesses both antitumor and antioxidation capabilities. Its chemoprotective actions are attributed partially to its anti-inflammation effect. The present study is aimed at checking the inhibitory actions of resveratrol on the release of mediators from bone marrow-derived mouse mast cells (BMMC) in vitro. Mast cells were prepared by isolating bone marrow cells from intact mice femora and culturing them for 4 weeks in the presence of IL-3 and FCS. The release reaction was triggered by IgE or calcium ionophore (A23187). Mediated by IgE, the release of histamine and tumor necrosis factor-alpha was significantly inhibited by resveratrol at a concentration of 100 microM; IgE-mediated release of leukotrienes and prostaglandin D (2) was also strongly suppressed at concentrations of 100 and 10 microM. Also, A23187-mediated release of histamine and leukotrienes release was strongly reduced by resveratrol at concentrations of 100 and 10 microM, respectively. Resveratrol exhibited its behavior without a significant cytotoxic activity against mast cells. In conclusion, resveratrol is a potent non-selective inhibitor of mediator release from activated mast cells and deserves further investigation of its biological modulations.
The ideal dose of Resveratrol has been a subject of debate for some time. The scientific community is coming to some agreement, that a dose between 200-300 mg optimizes health benefits for human use. Recent research in Italy revealed Resveratrol is particularly effective at stimulating hair growth when combined with Curcumin.
http://www.hairloss-research.org/UpdateSirtuin6-09.html
The Italian researchers who identified the apparent hair growth effects of an oral combination of Resveratrol and Curcumin stated rather nonspecifically in their patent application that Resveratrol by itself helped modify the hormonal environment in a way that was favorable for hair growth. Since Resveratrol is an established activator of Sirtuin 1, this study identifies a mechanism by which Resveratrol *may* do just that.
Mol Cell Biol. 2006 Nov;26(21):8122-35. Epub 2006 Aug 21
Hormonal control of androgen receptor function through SIRT1
Fu M, Liu M, Sauve AA, Jiao X, Zhang X, Wu X, Powell MJ, Yang T, Gu W, Avantaggiati ML, Pattabiraman N, Pestell TG, Wang F, Quong AA, Wang C, Pestell RG
Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA.
The NAD-dependent histone deacetylase Sir2 plays a key role in connecting cellular metabolism with gene silencing and aging. The androgen receptor (AR) is a ligand-regulated modular nuclear receptor governing prostate cancer cellular proliferation, differentiation, and apoptosis in response to androgens, including dihydrotestosterone (DHT). Here, SIRT1 antagonists induce endogenous AR expression and enhance DHT-mediated AR expression. SIRT1 binds and deacetylates the AR at a conserved lysine motif. Human SIRT1 (hSIRT1) repression of DHT-induced AR signaling requires the NAD-dependent catalytic function of hSIRT1 and the AR lysine residues deacetylated by SIRT1. SIRT1 inhibited coactivator-induced interactions between the AR amino and carboxyl termini. DHT-induced prostate cancer cellular contact-independent growth is also blocked by SIRT1, providing a direct functional link between the AR, which is a critical determinant of progression of human prostate cancer, and the sirtuins.
Conclusion
Over the past decade, SIRT1 has been the most investigated gene involved in diverse cellular functions. In the case of Androgen mediated disorders such as acne, BPH, and MPB, SIRT1 binds to and deacetylates the androgen receptor and represses dihydrotestosterone-induced androgen receptor signaling in humans.
The link betweenSIRT1 and both cancer, aging and androgen mediated disorders provide new insight into the therapeutic potential of small molecule activators or specific targets of SIRT1 for their prevention and treatment.
Resveratrol is a SIRT 1 activator that produces the same health benefits as Caloric restriction, which reliably prevents and/or corrects age related hair loss in rat studies.
SIRT1 has dependent diseases. One consistent observation has been that calorie restricted rats have robustly healthy coats of fur compared to controls. The SIRT1 activator resveratrol mimics the health benefits of CR and has emerged as a major drug development target for treating age-related disorders and aging in general.
Prostaglandin D2 (or PGD2) is a prostaglandin that is central to development of dermatologic inflammation, pattern hair loss, and allergic disorders, such as asthma.
A newly released, 2012 study showed a cause and effect relationship between abnormally high levels of PGD2 and male pattern baldness. With topical application they found PGD2 prevents hair growth, and mice who were genetically predisposed to produce higher levels of PGD2 had diminished hair growth. They additionally discovered PGD2 levels were much elevated in balding scalp versus non-balding scalp tissue. The study concluded that one of the receptors involved in production of PGD2, GPR44, constituted a precise therapeutic target for hormonal hair loss in both men and women.
Sci Transl Med. 2012 Mar 21; 4(126):126ra34.
Prostaglandin D2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia.
Garza LA, Liu Y, Yang Z, Alagesan B, Lawson JA, Norberg SM, Loy DE, Zhao T, Blatt HB, Stanton DC, Carrasco L, Ahluwalia G, Fischer SM, FitzGerald GA, Cotsarelis G.
Source
Department of Dermatology, Kligman Laboratories, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Abstract
Testosterone is necessary for the development of male pattern baldness, known as androgenetic alopecia (AGA); yet, the mechanisms for decreased hair growth in this disorder are unclear. We show that prostaglandin D(2) synthase (PTGDS) is elevated at the mRNA and protein levels in bald scalp compared to haired scalp of men with AGA. The product of PTGDS enzyme activity, prostaglandin D(2) (PGD(2)), is similarly elevated in bald scalp. During normal follicle cycling in mice, Ptgds and PGD(2) levels increase immediately preceding the regression phase, suggesting an inhibitory effect on hair growth. We show that PGD(2) inhibits hair growth in explanted human hair follicles and when applied topically to mice. Hair growth inhibition requires the PGD(2) receptor G protein (heterotrimeric guanine nucleotide)-coupled receptor 44 (GPR44), but not the PGD(2) receptor 1 (PTGDR). Furthermore, we find that a transgenic mouse, K14-Ptgs2, which targets prostaglandin-endoperoxide synthase 2 expression to the skin, demonstrates elevated levels of PGD(2) in the skin and develops alopecia, follicular miniaturization, and sebaceous gland hyperplasia, which are all hallmarks of human AGA. These results define PGD(2) as an inhibitor of hair growth in AGA and suggest the PGD(2)-GPR44 pathway as a potential target for treatment.
Because PGD2's correlation with asthma is well established, several drugs that down regulate PGD2 are already in clinical trials. PGD2 inhibitors would serve to promote hair growth. Scientists involved in this study, including Dr. Cotsarelis of stem cell research renown, state that they’ve already formulated pills containing the vital PGD2 blocking properties. But why wait for an expensive, patented medication. Resveratrol has been shown to significantly suppress PGD2 at low concentrations readily obtainable through oral dosing, as evidenced by the abstract presented below. Oral resveratrol has also been shown to have anti-asthmatic effects superior to that of dexamethasone, the side effect wrought, cortico-steroid of choice for managing asthma symptoms.
Planta Med. 2004 Apr;70(4):305-9.
Resveratrol inhibits the release of mediators from bone marrow-derived mouse mast cells in vitro.
Baolin L, Inami Y, Tanaka H, Inagaki N, Iinuma M, Nagai H.
Source
Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, P. R. China.
Abstract
Resveratrol is a natural phytoalexin occurring in grapes, vines and peanuts and possesses both antitumor and antioxidation capabilities. Its chemoprotective actions are attributed partially to its anti-inflammation effect. The present study is aimed at checking the inhibitory actions of resveratrol on the release of mediators from bone marrow-derived mouse mast cells (BMMC) in vitro. Mast cells were prepared by isolating bone marrow cells from intact mice femora and culturing them for 4 weeks in the presence of IL-3 and FCS. The release reaction was triggered by IgE or calcium ionophore (A23187). Mediated by IgE, the release of histamine and tumor necrosis factor-alpha was significantly inhibited by resveratrol at a concentration of 100 microM; IgE-mediated release of leukotrienes and prostaglandin D (2) was also strongly suppressed at concentrations of 100 and 10 microM. Also, A23187-mediated release of histamine and leukotrienes release was strongly reduced by resveratrol at concentrations of 100 and 10 microM, respectively. Resveratrol exhibited its behavior without a significant cytotoxic activity against mast cells. In conclusion, resveratrol is a potent non-selective inhibitor of mediator release from activated mast cells and deserves further investigation of its biological modulations.
The ideal dose of Resveratrol has been a subject of debate for some time. The scientific community is coming to some agreement, that a dose between 200-300 mg optimizes health benefits for human use. Recent research in Italy revealed Resveratrol is particularly effective at stimulating hair growth when combined with Curcumin.
http://www.hairloss-research.org/UpdateSirtuin6-09.html
The Italian researchers who identified the apparent hair growth effects of an oral combination of Resveratrol and Curcumin stated rather nonspecifically in their patent application that Resveratrol by itself helped modify the hormonal environment in a way that was favorable for hair growth. Since Resveratrol is an established activator of Sirtuin 1, this study identifies a mechanism by which Resveratrol *may* do just that.
Mol Cell Biol. 2006 Nov;26(21):8122-35. Epub 2006 Aug 21
Hormonal control of androgen receptor function through SIRT1
Fu M, Liu M, Sauve AA, Jiao X, Zhang X, Wu X, Powell MJ, Yang T, Gu W, Avantaggiati ML, Pattabiraman N, Pestell TG, Wang F, Quong AA, Wang C, Pestell RG
Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA.
The NAD-dependent histone deacetylase Sir2 plays a key role in connecting cellular metabolism with gene silencing and aging. The androgen receptor (AR) is a ligand-regulated modular nuclear receptor governing prostate cancer cellular proliferation, differentiation, and apoptosis in response to androgens, including dihydrotestosterone (DHT). Here, SIRT1 antagonists induce endogenous AR expression and enhance DHT-mediated AR expression. SIRT1 binds and deacetylates the AR at a conserved lysine motif. Human SIRT1 (hSIRT1) repression of DHT-induced AR signaling requires the NAD-dependent catalytic function of hSIRT1 and the AR lysine residues deacetylated by SIRT1. SIRT1 inhibited coactivator-induced interactions between the AR amino and carboxyl termini. DHT-induced prostate cancer cellular contact-independent growth is also blocked by SIRT1, providing a direct functional link between the AR, which is a critical determinant of progression of human prostate cancer, and the sirtuins.
Conclusion
Over the past decade, SIRT1 has been the most investigated gene involved in diverse cellular functions. In the case of Androgen mediated disorders such as acne, BPH, and MPB, SIRT1 binds to and deacetylates the androgen receptor and represses dihydrotestosterone-induced androgen receptor signaling in humans.
The link betweenSIRT1 and both cancer, aging and androgen mediated disorders provide new insight into the therapeutic potential of small molecule activators or specific targets of SIRT1 for their prevention and treatment.
Resveratrol is a SIRT 1 activator that produces the same health benefits as Caloric restriction, which reliably prevents and/or corrects age related hair loss in rat studies.
SIRT1 has dependent diseases. One consistent observation has been that calorie restricted rats have robustly healthy coats of fur compared to controls. The SIRT1 activator resveratrol mimics the health benefits of CR and has emerged as a major drug development target for treating age-related disorders and aging in general.
kapa
Μέλος του προσωπικού
ψηνεται κανεις που εχει τριχοπτωση για δοκιμη? :18m:
http://www.hairloss-research.org/UpdateSirtuin6-09.html
http://www.hairloss-research.org/UpdateGrapeseedHairlossMechanism9-09.html
http://www.hairloss-research.org/UpdateResveratrolandMenopausalHairloss1-10.html
http://www.hairloss-research.org/UpdateNeurotrophin7-11.html
http://www.hairloss-research.org/UpdatePDG7-12.html
η ρεσβερατρολη εχει παρα πολλες πιθανοτητες να μειωσει την τριχοπτωση.
σε καμια περιπτωση regrowth,τα παραλενε λιγο οι ερευνες.
εχει αντικαρκινικες ιδιοτητες.και βελτιωση αγγειακου συστηματος
πολυ πιο μετα θα ακολουθησω και εγω.
προσοχη μονο οσοι χρησιμοποιουν υπερτασικα φαρμακα
http://www.hairloss-research.org/UpdateSirtuin6-09.html
http://www.hairloss-research.org/UpdateGrapeseedHairlossMechanism9-09.html
http://www.hairloss-research.org/UpdateResveratrolandMenopausalHairloss1-10.html
http://www.hairloss-research.org/UpdateNeurotrophin7-11.html
http://www.hairloss-research.org/UpdatePDG7-12.html
η ρεσβερατρολη εχει παρα πολλες πιθανοτητες να μειωσει την τριχοπτωση.
σε καμια περιπτωση regrowth,τα παραλενε λιγο οι ερευνες.
εχει αντικαρκινικες ιδιοτητες.και βελτιωση αγγειακου συστηματος
πολυ πιο μετα θα ακολουθησω και εγω.
προσοχη μονο οσοι χρησιμοποιουν υπερτασικα φαρμακα