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

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

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 (P<0.05), but there was no difference in IMT of carotid artery and other blood biochemical indicators between the 2 groups (P>0.05). 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.

ObjectiveTo investigate the efficacy of different methods of anesthesia for laparoscopic hysterectomy.MethodsSixty ASA Ⅰ or Ⅱ patients,aged 45-60 yr,weighing 55-65 kg,scheduled for laparoscopic hysterectomy,were equally and randomly divided into 2 groups:combined intravenous-inhalational anesthesia group (group Ⅰ ) and combined spinal-epidoral anesthesia (CSEA) + general anesthesia group (group Ⅱ ).In group Ⅰ,anesthesia was maintained with inhalation of sevoflurane and infusion of remifentanil after induction of anesthesia.In group Ⅱ,CSEA was performed,after the upper level of sensory block was stable,general anesthesia was induced and maintained with inhalation of sevoflurane,and state entropy (SE) was naintained at 45-60.Arterial blood samples were taken to determine the plasma concentrations of adrenaline ( AE ),norepinephrine (NE) and dopamine (DA) after admission to the operation room,after completion of pneumoperitoneum,at 10 min after pneumopentoneum,during uterus traction,during removal of the laryngeal mask airway,and at 10 min after removal of the laryngeal mask airway (T0-5).The time for recovery of spontaneous breathing,extubation time,and time of regaining consciousness were recorded at the end of operation.The side-effects and number of patients requiring increments of analgesics were also recorded within 48 h after operation.Patient' s satisfaction was recorded at 48 h after operation.ResultsCompared with group Ⅰ,the plasma concentrations of AE and NE at T3-5 and the plasma concentrations of DA at T3,5 were significantly decreased,the time for recovery of spontaneous breathing,extubation time,and time of regaining corsciousess were significantly shortened,and the incidence of agitation and the number of patients requiring increments of analgesics were significantly decreased in group Ⅱ ( P ＜0.05).There was no significant difference in the incidence of intraoperative awareness,and nausea and vomiting after operation,and the level of patient' s satisfaction at 48 h after operation between the two groups ( P ＞ 0.05).ConctusionCSEA + general anesthesia has better efficacy than combined intravenous-inhalational anesthesia when used for laparoscopic hysterectomy.

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

Objective To observe the possible anti-inflammatory and anti-angiogenesis effects of iguratimodon human synovial fibroblast cell line MH7A derived from patients with rheumatoid arthritis (RA).Methods MH7A cells were stimulated with interleukin (IL)-1β and treated simult aneously or sequenti-ally with different concentrations of iguratimod and methotrexate (MTX).Release of vascular endothelial growth factor (VEGF), endostatin (ES) and tumour necrosis factor-α (TNF-α) was quantified by enzyme linked immunosorbent assay (ELISA).The statistics software SPSS 13.0 was used for statistical analyses.The experimental data were analyzed in terms of variance analysis and LSD test.In all cases, a P value lower than 0.05 was considered significant.Results The concentrations of VEGF, ES and TNF-α of the control group were (57±98) pg/ml, (924±39) pg/ml, (16.40±6.08) pg/ml respectively, while those of the experimental group were (1 155±177) pg/ml, (295±35) pg/ml and (36.90±3.54) pg/ml respectively.The differences of VEGF (t=9.092, P＜0.01) and ES (t=19.685, P＜0.01) between the control group and the experimental group was statistically significant.There was significant difference in the levels of TNF-α between the two groups (t=2.495, P＜0.05).VEGF of the iguratimod groups was (640±127) pg/ml in the iguratimod group (100 μmol/L), (787±172) pg/ml in the iguratimod group (25 μmol/L), and (776±99) pg/ml in the iguratimod group (6.25 μmol/L).VEGF of the MTX groups was (1 322±264) pg/ml in the MTX group (100 μmol/L), (1 071±63) pg/ml in the MTX group (25 μmol/L), and (863±70) pg/ml in the MTX group (6.25 μmol/L).All concentration of the iguratimod groups could effectively reduce the expression of VEGF in MH7A cells.Compared with the experimental group, the difference was statistically significant (100 μmol/L group: t=4.264, P＜0.01;25 μmol/L group: t=3.045, P＜0.01;6.25 μmol/L group: t =3.132, P ＜0.01).MTX (6.25 μ mol/L) could reduce the expression of VEGF in MH7A cells.Compared with the experimental group, the difference was statistically significant (t=2.415,P＜0.05).ES of the iguratimod groups was (979±30) pg/ml in the iguratimod group (100 μmol/L), (842±14)pg/ml in the iguratimod group (25 μmol/L), and (485 ±72) pg/ml in the iguratimod group (6.25 μmol/L).ES of the MTX group was (934±23) pg/ml in the MTX (100 μmol/L) group, (825±28) pg/ml in the MTX group (25 μmol/L), and (772 ±44) pg/ml in the MTX group (6.25 μmol/L).Both iguratimod and MTX groups effectively increased the expression of ES in MH7A cells.Compared with the experimental group, the difference was statistically significant (100 μmol/L group: t=21.387, P＜0.01;25 μmol/L group: t=17.122,P＜0.01;6.25 μmol/L group: t=5.929, P＜0.01).The expression of ES of the iguratimod group (100 μmol/L)and iguratimod group(25 μmol/L) was higher than that of the iguratimod group (6.25 μmol/L).The difference was statistical significant(100 μmol/L group: 6.25 μmol/L group was t=15.458,P＜0.01;100 μmol/L group: 6.25 μ mol/L group was t=11.193, P＜0.01).The expression of ES of the iguratimod group(6.25 μmol/L) was lower than that of the MTX group (6.25 μmol/L).The difference was statistically significant (t=9.001, P＜0.01).TNF-α was (4.73 ±1.15) pg/ml in the iguratimod group (100 μmol/L), (4.40±2.65) pg/ml in the iguratimod group (25 μmol/L), and (4.40±0.10) pg/ml in the iguratimod group (6.25 μmol/L).TNF-α of the MTX groups were (4.40±3.61) pg/ml in the MTX group (100 μ mol/L), (13.40±16.46) pg/ml in the MTX group (25 μmol/L),and (21.73±16.50) pg/ml of the MTX group (6.25 μmol/L).Both the iguratimod groups and the MTX group (100 μmol/L) effectively reduced the expression of TNF-α in MH7A cells.Compared with the experimental group, the difference was statistically significant(100 μmol/L group: t=3.914, P＜0.01;25 μ mol/Lgroup: t=3.955,P＜0.01;6.25 μ mol/L group: t=3.955, P＜0.01).Theexpression of TNF-α of the MTX groups (100 μ mol/L and 25 μmol/L) reduced significantly.Compared with the experimental group, the difference was statistically significant (100 μmol/L group: t=3.955, P＜0.01;25 μmol/L group: t=2.859, P＜0.05).The expression of TNF-αof the iguratimod group (6.25 μmol/L) was lower than that of the MTX group (6.25 μmol/L).The difference was statistical significant (t=2.359, P＜0.05).Conclusion Iguratimod presents strong anti-inflammatory and antiangiogenesis properties.This study provides insight into the possible molecular mechanisms of iguratimod and suggests that it can be a medication for the treatment of chronic inflammatory diseases like RA.

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.

Objective To observe the effects of iguratimod ( IT) combined with methotrexate ( MTX) in patients with refractory rheumatoid arthritis ( rRA) . Methods Sixty patients with rRA were randomly divided into 2 groups ( n=30 each group) . The cases in treatment group received 50 mg.d-1 of iguratimod and 10 mg of MTX for 16 weeks. The cases in control group were treated by 10-15 mg of MTX. DAS28 was analyzed. Levels of VEGF and endostatin ( ES) were quantified. Results In the treatment group,after 16-week treatment,DAS28,levels of VEGF and ES were (3.0±1.2),(818.9±178.8) pg.mL-1, (337.8±132.6) ng.mL-1,and those in the control group were (5.7±1.9),(1000.2±245.9) pg.mL-1,(253.8±77.8) ng.mL-1,respectively. In the treatment group,DAS28 and VEGF after the treatment were significantly decreased as compared with those before the treatment ( P<0.01) . The decrement was more significant in the treatment group than in the control group ( P<0.01) . At the 16th week of treatment,ES was significantly increased as compared with that before the treatment ( P<0.01) , and there was a significant difference between the treatment group and the control group (P<0.01). Conclusion Iguratimod combined with MTX have a prominent effect on rRA with high safety. The efficacy of IT on RA might be related with decreasing VEGF release,increasing ES production and alleviating synovium angiogenesis.