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.



Department of Dermatology, Kligman Laboratories, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.


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.


Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, P. R. China.


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.