Gamma-linolenic acid attenuates experimental pulmonary fibrosis in hamsters.

Abstract

Although bleomycin (BLM), an antineoplastic drug, is used in the treatment of a variety of tumors, the mechanism(s) that contribute to its induced lung injury and fibrosis are not fully elucidated. Since alterations in the levels of certain fatty acid metabolites have been associated with BLM-induced lung injury, we tested the effects of dietary gamma-linolenic acid (GLA)-containing evening primrose oil on BLM-induced morphological alterations in the hamster lung, the marked elevation of tissue hydroxyproline (a marker for collagen synthesis), and elevated generation of arachidonic acid metabolites (marker of inflammatory mediators). Our data revealed that after 14 d of dietary GLA-containing oil (i) BLM-induced elevation of lung hydroxyproline was suppressed (P < 0.05), (ii) the marked BLM-induced elevation of lung leukotriene B4 (LTB4) (a marker of polymorphanuclear generation of proinflammatory LTB4) was significantly suppressed (P < 0.05). The decrease in LTB4 was accompanied by marked elevations (P < 0.05) of lung prostaglandin E1 (PGE1) and 15-hydroxyeicosatrienoic acid (15-HETrE), both with known antiinflammatory properties. Taken together, data from these studies suggest that dietary GLA-containing oil contributes to tissue elevation of PGE1 and 15-HETrE, which in vivo may attenuate lung inflammation and fibrosis.