pge2 การใช้

• PGE2 and prostacyclin inhibit platelet aggregation and dilate blood vessels.
• This elevates levels of PGE2, sensitizing pain neurons ".
• PGE2 is the ultimate mediator of the febrile response.
• The negative effect of hyperinsulinemia on prostaglandin PGE1 / PGE2 balance may be significant.
• Up-regulation of PGE2 has been implicated as a possible cause of nail clubbing.
• It has been shown that sertaconazole activatates of the p38 / COX2 / PGE2 pathway.
• The set point temperature of the body will remain elevated until PGE2 is no longer present.
• PGE2 also suppresses T cell receptor signaling and may play a role in resolution of inflammation.
• This enzyme catalyses the synthesis of PGE2 from PGH2 ( produced by cyclooxygenase from arachidonic acid ).
• A trigger of the fever, called a pyrogen, causes a release of prostaglandin E2 ( PGE2 ).
• Since elevated PGE2 levels are correlated with PDP, urinary PGE2 can be a useful biomarker for this disease.
• Since elevated PGE2 levels are correlated with PDP, urinary PGE2 can be a useful biomarker for this disease.
• Prostaglandins, specifically PGE2 and PGI2, are important in inflammation and have been implicated in promoting apical resorption.
• The conversion rate of omega-6 DGLA to AA largely determines the production of the prostaglandins PGE1 and PGE2.
• PGE2 acts on neurons in the preoptic area ( POA ) through the prostaglandin E receptor 3 ( EP3 ).
• PGE2 can have a variety of important effects in the body including activation of the body's fever response.
• MRP4 / ABCC4 also transports prostaglandins, for example PGE2, out of the cell where they can bind receptors.
• This leads to a reduction in the release of inflammatory mediators, principally oxygen free radicals and prostaglandins ( PGE2, PGF2a ).
• The inflammatory response is enhanced by the use of vasodilators, including prostaglandin E1 ( PGE, ) and PGE2 and inhibited by vasoconstrictors.
• Inhibition of PTGS1 ( COX-1 ) reduces the basal production of cytoprotective PGE2 and PGI2 in the stomach, which may contribute to gastric ulceration.