Prostaglandin biosynthesis by human skin and its inhibition by corticosteroids.
Homogenates of human breast skin form prostaglandins E(2) and F(2alpha) in the presence of arachidonic acid substrate. Significant inhibition of biosynthesis of prostaglandin E(2) and F(2alpha) was observed in the presence of the anti-inflammatory corticosteroid fluocinolone acetonide. This effect was dose-related. By contrast no significant inhibition was observed in the presence of an approximately equimolar concentration of hydrocortisone.Since prostaglandins have been recovered from several types of inflammatory reactions and are capable of mediating most of the components of inflammation the possibility arises that corticosteroids may owe their anti-inflammatory activity at least in part to inhibition of prostaglandin biosynthesis.
D001095:Arachidonic Acids / Q000378:metabolism; D001940:Breast; D004305:Dose-Response Relationship, Drug; D005260:Female; D005446:Fluocinolone Acetonide / Q000494:pharmacology*; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology; D066298:In Vitro Techniques; D011453:Prostaglandins / Q000096:biosynthesis*; D012867:Skin / Q000187:drug effects / Q000378:metabolism*
D001095:Arachidonic Acids; D011453:Prostaglandins; D005446:Fluocinolone Acetonide; D006854:Hydrocortisone