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Objective:To observe the effect of pioglitazone on carotid artery intima-media thickness (IMT) and plaque-positive rate in patients with metabolic syndrome, and to ifnd a new way to improve arterial remodeling in patients with metabolic syndrome. Methods:Patients with metabolic syndrome were randomly divided into a control group (n=60) and a pioglitazone group (n=61). All subjects received basic therapeutic measures, i.e, appropriate medication to control blood pressure, blood sugar and cholesterol. Pioglitazone (15 mg/d) was given to patients in the pioglitazone group, and placebo (vitamin C) in the control group for 24 weeks. Color doppler ultrasound was used to measure carotid artery IMT and plaque-positive rate of patients in the 2 groups atfer the intervention. Japan’s Hitachi 7600-020 automatic biochemical analyzer was used to measure fasting serumal triglycerides, total cholesterol, high density lipoprotein cholesterol, low-density lipoprotein cholesterol, free fatty acids, fasting blood glucose, 2-hour postprandial glucose and liver and kidney function, etc. The differences between groups after the intervention were analyzed and compared in IMT, plaque-positive rate and all blood biochemical indicators. Results:Atfer the intervention, compared with the control group, carotid artery plaque-positive rate and the levels of triglyceride and free fatty acid decreased in the pioglitazone group (P0.05). Conclusion:Pioglitazone intervention can significantly improve pathologic artery remodeling, and it can more effectively inhibit the arterial plaque-formation than basic therapeutic measures in patients with metabolic syndrome.
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Objective To investigate the effects and mechanisms of rosiglitazone on the expressions of nuclear factor-κB and matrix metalloprotease (MMP-9) in peripheral blood monocyte-derived macrophages (MDMs) in patients with coronary heart disease. Method This was a clinical case-control study. Forty-eight actue coronary symdrome (ACS) patients (ACS group), and 20 patients with stable angina (SA) (control group) were collected. They were performed coronary arteriography in the Department of Cardiology of the Second Xiangya Hospital from March to April in 2007. Exclusion criteria included acute infection, trauma or surgery patients within four weeks, cerebral vascular accident, liver and kidney dysfunction, cancer, and so on. The peripheral blood mononuclear cells were isolated and transformed into MDMs with macrophage colony-stimulating factor treatment. The transformed MDMs were randomly assigned into subgrougs and incubated with 0 /μmol/L, 1 μmol/L, 10 μmol/L, 20 μmol/L of rosiglitazone respectively. The expressions of PPAR-γ mRNA, MMP-9 mRNA were determined by RT-PCR and nuclear factor-κB P65 (NF-KB P65) expression by immunohistochemistry. Multiple comparisons were examined for significant differences using analysis of variance (ANOVA). Results The basal expression of PPAR-y mRNA was lower, in contrast, the levels of NF-KB P65 and MMP-9 mRNA were higher in ACS group than control group. PPAR-γ mRNA expression were significantly upregulated in both ACS and control groups with rosiglitazone treatment. PPAR-γ mRNA expression was positive correlation, while the expressions of MMP-9 mRNA were negative correlation with the rosiglitazone concentration in the ACS group. Rosiglitazone inhibited the expression of NF-KB in a concentration-independent manner in ACS and control groups. Conclusions The expression of PPAR-y mRNA is inhibited, while the activity of NF-KB and expression of MMP-9 mRNA are enhanced in MDMs of ACS cases. Rosiglitazone intervention may inhibit NF-KB activity and MMP-9 expression by upregulation of PPAR-y expression in MDMS of patiens with ACS.
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Background Fractalkine(FKN) is a novel chemokine that mediate the adhesion of monocyte to vascular endothelial cell,involving in the development of atherosclerosis(AS).Objective To investigate the effect of interleukin-18(IL-18) on the fractalkine expression in human umbilical vascular endothelial cells(HUVEC),and the role of fractalkine in the monocytes THP-1 adhesion on HUVEC.Methods Fractalkine expression in HUVEC was determined by reverse transcription-polymerase chain reaction(RT-PCR),and the adhesion of THP-1 to HUVEC was assessed by Flow Chamber.Results Incubation of HUVEC with IL-18 upregulated FKN mRNA expression in dose-dependent manner.In the concentration of IL-18 ranged 0,25,50,100 ?g/L,the FKN mRNA was increased from(0.10?0.01),(0.49?0.04),(0.63?0.09) to(0.85?0.07)(P trend
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BACKGROUND:Oxidized low-density lipoprotein(ox-LDL) is recognized as the essential condition for atherosclerosis.As the ox-LDL-specific receptor,oxidized low-density lipoprotein receptor-1(LOX-1) involved in vascular inflammation and plaques develop-ment of the process.OBJECTIVE:To investigate the effect of fluvastatin on the expression of LOX-1 in human umbilical vein endothelial cells(HUVECs) induced by ox-LDL.DESIGN,TIME AND SETTING:The comparative observation was completed in the Medical Center of Second Xiangya Hospital,Central South University between August 2006 and May 2007.MATERIALS:Human umbilical vein endothelial cell line was purchased from the America ATCC Company.Fluvastatin original powder was supplied by Beijing Novartis Pharmaceutical Co.,Ltd.METHODS:HUVECs were incubated with:①Stimulation by ox-LDL with end concentration of 25,50,100 mg/L.②LOX-1 neutralizing antibody,and interfered with 50 mg/L ox-LDL.③Interfered with nuclear factor-?B(NF-?B) blockers pyrrolidine dithiocarbamate(PDTC),followed by 50 mg/L ox-LDL intervention.④Fluvastatin with concentration of 0.01,0.1,1 ?mol/L were used to interfere the cells,followed by 50 mg/L ox-LDL intervention.⑤There was an blank group as the control.MAIN OUTCOME MEASURES:The expression of LOX-1 mRNA level was detected by RT-PCR.RESULTS:The levels of mRNA of LOX-1 were increased after cells had beenwere incubated with different concertrations of ox-LDL,when compared with the control group.Within the dosage range of 25 to 50 mg/L,the above-mentioned indexes significantly changed in a concentration-dependent manner(P
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Aim To investigate the effect of simvastatin on the FKN expression in human umbilical vascular endothelial cells(HUVEC)up-regulated by interleukine-18(IL-18),and the effect on adhesion of FKN to monocyte THP-1.Methods FKN expression in HUVEC was determined by reverse transcription-polymerase chain reaction (RT-PCR), and the adhesion was checked by in vitro Flow chamber.Results Incubation of HUVECs with IL-18 upregulated FKN mRNA expression(P