Aim: To investigate the protective effects of prostaglandin E 1 (PGE 1 ) against H 2 O 2 -induced oxidative damage on human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were pretreated with PGE 1 (0.25, 0.50, and 1.00 µmol/L) for 24 h and exposed to H 2 O 2 (200 µmol/L) for 12 h, and cell viability was measured by the MTT assay. LDH, NO, SOD, GSH-Px, MDA, ROS, and apoptotic percentage were determined. eNOS expression was measured by Western blotting and real-time PCR. Results: PGE 1 (0.25−1.00 µmol/L) was able to markedly restore the viability of HUVECs under oxidative stress, and scavenged intracellular reactive oxygen species induced by H 2 O 2 . PGE 1 also suppressed the production of lipid peroxides, such as MDA, restored the activities of endogenous antioxidants including SOD and GSH-Px, and inhibited cell apoptosis. In addition, PGE 1 significantly increased NO content, eNOS protein, and mRNA expression. Conclusion: PGE 1 effectively protected endothelial cells against oxidative stress induced by H 2 O 2 , an activity that might depend on the up-regulation of NO expression.
Prostaglandin E1 (PGE1) is a member of the prostaglandins and has a variety of cardiovascular protective effects. Increasing attention has been paid to the anti-inflammation activity of PGE1, but little direct evidence has been found. We investigated the effects of PGE1 on cell adhesion and inflammation and the mechanisms responsible for this activity in tumor necrosis factor (TNF)-treated human umbilical vein endothelial cells. Results demonstrated that pretreatment with PGE1 decreased the adhesion between vascular endothelial cells and monocytes, reduced the expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and E-selectin in vascular endothelial cells. In addition, PGE1 suppressed TNF-induced NF-kappaB activation and production of reactive oxygen species. We concluded that PGE1 suppressed the vascular inflammatory process, which might be closely related to the inhibition of reactive oxygen species and NF-kappaB activation in human umbilical vein endothelial cells.
Background: The atherosclerotic process starts at an early age and is linked to obesity. However, the exact pathophysiological mechanism is poorly understood. Objective: To investigate the relationship between serum adiponectin and metabolic syndrome and early arteriosclerosis. Subjects: 176 obese and 88 normal children. Methods: Ultrasound measurement was performed to investigate IMT, FMD, carotid artery compliance (CAC). Adiponectin was measured by enzyme-linked immunosorbent assay. Results: Adiponectin levels correlated negatively with obese markers, blood pressure, fasting insulin, high sensitive CRP, HOMA-IR and IMT; marginally positively associated with CAC and HDL-c. The risk of metabolic syndrome increased 3.43 times when adiponectin levels were less than 7060ng/ml. Heavy obesity, hypertension, low HDL-c, fasting hyperinsulin, High LDL-c and metabolic syndrome percentage were different in three groups according to the cut-off value of adiponectin. Conclusions: Low adiponectin levels are associated with a high incidence of metabolic syndrome.
This study evaluated the effect of prostaglandin E1 (PGE1) on the stability of atherosclerotic plaque. A vulnerable plaque model was established in rabbits, using balloon injury combined with a high-cholesterol diet. The rabbits were distributed into a control group, a low-dose PGE1 treatment group, a moderate-dose PGE1 treatment group, a high-dose PGE1 treatment group, and a simvastatin treatment group, with treatments lasting for 4 weeks. At week 13 (at the end of the experiments), atherosclerotic plaque was triggered by injection of Russell's viper venom (Chinese) and histamine. Serological, pathological, immunohistochemical, and gene-expression studies were subsequently performed. PGE1 treatment did not alter serum lipid levels; however, PGE1 dose-dependently increased the thickness of the fibrous caps, and decreased the plaque vulnerability index. The plaque contents of macrophage- and the mRNA levels of monocyte-chemotactic protein-1, matrix metalloproteinase-1, and matrix metalloproteinase-9 were markedly reduced in all of the PGE1 treatment groups, with the high-dose of PGE1 being more effective than the simvastatin treatment. These findings suggest that PGE1 dose-dependently enhances the stability of atherosclerotic plaque. The high-dose of PGE1 presented more protection in terms of inhibiting macrophage accumulation and inflammatory expression in plaque. Our findings suggest a novel drug for the treatment of atherosclerosis.
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