Effects of altering the eicosanoid precursor pool on neovascularization and inflammation in the alkali-burned rabbit cornea.
The effects of altering the eicosanoid precursor pool on several aspects of the nonimmunologically mediated inflammatory and angiogenic processes that follow 1N and 4N NaOH alkali burning of the rabbit cornea were compared with controls. Diets were supplemented with several dosages of oils containing either gamma-linolenic acid (GLA) (borage oil), eicosapentaenoic acid (EPA) (sardine oil), or a combination of the two in a dose-response protocol. Significant changes in serum fatty acid composition were demonstrated. Gamma-linolenic acid proved consistently superior to EPA in modulating the neovascular response judged by three neovascular indices. At 14 days, GLA significantly reduced the polymorphonuclear leukocyte and macrophage inflammatory infiltrate and EPA reduced the macrophage component, both with high dose; EPA also reduced keratocyte proliferation. Wound-healing parameters were unaffected. Evidence for GLA-EPA synergism was modest. Prolonged neovascular responses and chronic inflammation occurring in the clinically relevant context of severe structural damage can be modulated by nutritional alteration of the eicosanoid precursor pool.[1]References
- Effects of altering the eicosanoid precursor pool on neovascularization and inflammation in the alkali-burned rabbit cornea. Ormerod, L.D., Garsd, A., Abelson, M.B., Kenyon, K.R. Am. J. Pathol. (1990) [Pubmed]
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