Effect of Flaxseed (Flaxseed/Linseed) Fixed Oil against Distrinct Phases of Inflammation

The present investigation summarizes the effect of Linum usitatissimum fixed oil against different phases of acute inflammatory reaction, namely, protein exudation, peritoneal capillary permeability, and leukocyte migration. The fixed oil exhibited dosedependent inhibition of protein exudation vascular permeability, comparable to standard aspirin. The oil also inhibited the leukocyte migration in pleural exudates in a dose-dependent manner. Production of less vasodilatory (PGE3) and chemotactic (LTB5) eicosanoids through EPA (derived from linolenic acid) metabolism could account for the above observations. (Authors abstract)

The antimicrobial activity of L. usitatissimum (flaxseed) oil and its therapeutic efficacy in bovine mastitis, an inflammatory disorder caused by microbial infection, has been reported recently. Considering the significant anti-inflammatory and antiarthritic activity, the present study has been undertaken to evaluate the possible effect of fixed oil against distinct phases of inflammation using suitable animal models. Flaxseed fixed oil demonstrated a significant dose dependent inhibition of protein exudation (i.e., rise in protein concentration in peritoneal fluid) and inhibited the vascular permeability evidenced by inhibition to dye leakage. Degree of inhibition of protein exudation and vascular permeability was comparable to standard aspirin. The present investigation revealed the effect of Flaxseed fixed oil on distinct phases of inflammatory process: firstly an acute phase of local vasodilatation and increased capillary permeability leading to exudation, followed by leucocytes migration.  Antiinflammatory potential was further confirmed by inhibition of carrageenan induced pleurisy in rats, as flaxseed fixed oil significantly inhibited the migration of leucocytes in pleural exudates.

ALA showed a significant oedema inhibition against all the inflammatory mediators tested suggesting the ALA as a dual inhibitor of arachidonate metabolism. ALA is a precursor for eicosapentaenoic acid (EPA), which competes with AA (20:4, n6, precursor for lipid mediators of inflammation) for cyclooxygenase and lipoxygenase pathway. EPA by acting as a substrate for cyclooxygenase and lipoxygenase pathway produces PGE3 (less potent vasodilator than PGE2) and LTB5 (100 times less potent chemotactic than LTB4). Thus, less vasodilatory (PGE3) and chemotactic (LTB5) response of lipid mediators derived from EPA (metabolic product of ALA metabolism) accounts for the inhibition of fluid and protein exudation along with diminished leucocytes migration observed in the present experiment. (Editors comments)