PGD2

AcronymDefinition
PGD2Prostaglandin D2
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References in periodicals archive ?
Lutz, "The mast cell mediator PGD2 suppresses IL-12 release by dendritic cells leading to Th2 polarized immune responses in vivo," Immunobiology, vol.
Early research in male pattern hair loss found that men with AGA have elevated levels of PGD2 in the balding scalp area.
The urinary PGD2 (Figure 1(b)), TXB2 (stable metabolite of TXA2) (Figure 1(c)), and 6-keto-PGF1[alpha] (stable metabolite of PGI2) (Figure 1(d)) were all remarkably increased in the db/db mice, which was unaffected by Rosi administration.
As prostaglandinas tem diversas acoes que incluem, por exemplo, o efeito vasodilatador observado quando a PGD2 e liberada de mastocitos ativados por estimulos alergicos ou inflamatorios.
Platelets have receptors for prostaglandins that play important modulatory functions, thromboxane receptors, prostacyclin(PGI2), PGD2 and PGE2 receptors and PGE2 are important prostaglandin receptors.
These studies have shown that many second-generation H1-receptor antagonists (considered potentially or minimally sedating) and third-generation H1-receptor antagonists (considered non-sedating) inhibit release or generation of multiple inflammatory mediators, including IL-4, IL-6, IL-8, and IL-13; PGD2; LTC4; tryptase; histamine; and the TNF-[alpha]-induced chemokine RANTES, as well as eosinophil chemo taxis and adhesion.
Inhibiting PGD2 would disrupt the production of osteopontin.
D-type prostaglandin 2 (PGD2) is also synthesized from ARA by COXs and two types of PGD synthase and is nonenzymatically metabolized into 15-deoxy[[DELTA].sup.12,14]- prostaglandin [J.sub.2] (15d-[PGJ.sub.2]), which also promoted the proliferation of cultured embryonic NSPCs and postnatal NSPCs in the hippocampus [114].
Recently, BCA was found to be a potent, selective, and orally active prostaglandin D2 (PGD2) 4 receptor antagonist [15].
LPS by the receptor CD14, activates Kupffer cells to produce prostaglandin D2 and E2 (PGD2, PGE2), reactive nitrogen and oxygen species (RNS, ROS), endothelin-1 (ET-1), tumor necrosis factor-a (TNF-alpha), and interleukin 1 and 6 (IL-1, IL-6), resulting in the hypermetabolic liver state [1, 8].