出版社：American Society for Biochemistry and Molecular Biology
摘要：Severe endothelial abnormalities are a prominent feature in sepsis with cytokines such as tumor necrosis factor (TNF)α being implicated in the pathogenesis. As mimic to inflammation, human umbilical vascular endothelial cells (HUVEC) were incubated with TNFα for 22 h, in the absence or presence of the ω-6 fatty acid (FA), arachidonic acid (AA), or the alternative ω-3 FA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). TNFα caused marked alterations in the PUFA profile and long chain PUFA content of total phospholipids (PL) decreased. In contrast, there was a compensatory increase in mead acid [MA, 20:3(ω-9)], the hallmark acid of the essential fatty acid deficiency (EFAD) syndrome. Corresponding changes were noted in phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and phosphatidylinositol, but not in the sphingomyelin fraction. Supplementation with AA, EPA, or DHA markedly increased the respective FA contents in the PL pools, suppressed the increase in MA, and resulted in a shift either toward further predominance of ω-6 or predominance of ω-3 FA. We conclude that short-term TNFα incubation of HUVEC causes an EFAD state hitherto only described for long-term malnutrition, and that endothelial cells are susceptible to differential influence by ω-3 versus ω-6 FA supplementation under these conditions.
