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Aims: Cyclooxygenase- 2(COX- 2)- mediated prostaglandin production by activated macrophages is associated with inflammation and atherosclerosis. We investigated the relationship between COX- 2- mediated prostaglandin- E2(PGE2) release, cardiovascular risk factors, and carotid atherosclerosis in apparently healthy subjects. Methods and results: PGE2 release by lipopolysaccharide- stimulated blood monocytes was measured by ELISA in 291 subjects(76.5% men, mean age 58) who underwent global vascular risk assessment and carotid ultrasonography. COX- 2 expression(real- time RT- PCR) was analysed in a subgroup of 100 subjects(76% men, mean age 59). Inducible PGE2 production was associated with smoking and diabetes(P< 0.05), but not with arterial hypertension, dyslipidaemia, or obesity. Subjects in the highest tertile of PGE2(>8.1 ng/mL) had significantly higher mean carotid intima- media thickness(IMT) than those in the lowest tertile(P< 0.01). No significant differences among tertiles were observed in the levels of inflammatory markers(C- reactive protein, fibrinogen, and von Willebrand factor). The association between PGE2 and carotid IMT remained statistically significant(P=0.012) after adjustment for a number of cardiovascular and inflammatory risk factors. A correlation between COX- 2 expression and PGE2 production was observed(P< 0.005). Conclusions: COX- 2- mediated PGE2 overproduction by stimulated monocytes might provide a new marker of subclinical atherosclerosis in asymptomatic subjects exposed to cardiovascular risk factors.
Aims: Cyclooxygenase-2 (COX-2) - mediated prostaglandin production by activated macrophages is associated with inflammation and atherosclerosis. We investigated the relationship between COX- 2-mediated prostaglandin-E2 (PGE2) release, cardiovascular risk factors, and carotid atherosclerosis in apparently healthy subjects. Methods and results: PGE2 release by lipopolysaccharide-stimulated blood monocytes was measured by ELISA in 291 subjects (76.5% men, mean age 58) who underwent global vascular risk assessment and carotid ultrasonography. COX- 2 expression (real- time Inducible PGE2 production was associated with smoking and diabetes (P <0.05), but not with arterial hypertension, dyslipidaemia, or obesity. Subjects in the highest tertile of PGE2 (> 8.1 ng / mL) had significantly higher mean carotid intima-media thickness (IMT) than those in the lowest tertile (P <0.01). No significant differences among tertiles were o The association between PGE2 and carotid IMT was relatively pure (P = 0.012) after adjustment for a number of cardiovascular and inflammatory risk factors. A correlation between COX-2 expression and PGE2 production was observed (P <0.005). Conclusions: COX- 2-mediated PGE2 overproduction by stimulated monocytes might provide a new marker of subclinical atherosclerosis in asymptomatic subjects exposed to cardiovascular risk factors.