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Shui-ping Zhao

Publications and source records attributed to Shui-ping Zhao.

33 records · Page 2Linked to original sources
PubMed2005

[Atorvastatin reduces the expression of COX-2 mRNA in peripheral blood monocytes in patients with acute myocardial infarction and modulates the early inflammatory response].

OBJECTIVE: To measure the effect of atorvastatin on COX-2 expression in monocytes in patients with acute myocardial infarction (AMI). METHODS: Forty patients with AMI (AMI group) and 18 patients with stable coronary heart disease (control group) were enrolled, and patients with AMI were randomly given routine therapy (n = 20) and routine therapy plus atorvastatin (20 mg/day, n = 20) for a week. Peripheral blood monocytes for each participant including patients with AMI were isolated and cultured for 24 hours. During the culture, monocytes in patients with pretreatment AMI were incubated with celecoxib in different concentration (0, 0.1, 1 and 10 micromol/L). COX-2 mRNA expression in monocytes was measured by reverse transcription polymerase chain reaction (RT-PCR); concentrations of interleukin-6 (IL-6) in supernatant from monocytes and plasma hs-CRP levels were measured by using enzyme-linked immunosorbent assay (ELISA). RESULTS: COX-2 expression in monocytes in patients with AMI (0.92 +/- 0.13) was significantly higher than that in the control subjects (0.19 +/- 0.08), and decreased by 66% after atorvastatin (compared with that on routine therapy, P < 0.05); IL-6 secretions of monocytes in the AMI group (204.8 +/- 45.6 ng/L) increased dramatically compared with those in the control group (40.9 +/- 1.2 ng/L, P < 0.05), and reduced dramatically by 58% when incubated with 10 micromol/L celecoxib (P < 0.05) in a concentration-dependent manner; plasma levels of CRP in the AMI group (43.3 +/- 14.9 mg/L) significantly increased compared with those in the control group (1.7 +/- 0.8 mg/L), and reduced by 62% after atorvastatin (compared with those in the routine therapy group, P < 0.05). COX-2 expression in monocytes in the AMI group was positively correlated with both secretions of IL-6 and plasma level of CRP (r = 0.636 and 0.662, respectively, both P < 0.05). CONCLUSIONS: There is an inflammatory activation in peripheral blood monocytes in patients with early AMI, and the monocytes-derived COX-2 may play an important role in promoting early inflammatory process. Atorvastatin may decrease COX-2 expression in peripheral blood monocytes in patients with AMI and cyclooxygenase-dependent pathway might be correlated with the anti-inflammation mechanism of statin.

Aged↗
PubMed2004

[Changes and relations of soluble plasma CD40L and matrix metalloproteinase-9 levels in patients with coronary heart disease].

OBJECTIVE: To investigate the serum soluble CD40 ligand (sCD40L) levels in coronary heart disease and its relationship with MMP-9 and to explore the potential predicting factor for the acute coronary syndrome. METHODS: Enzyme-linked immunosorbent assay was used to measure the sCD40L and MMP-9 in 79 patients with coronary heart disease. RESULTS: sCD40L level was significantly higher in patients with acute coronary syndrome [(1.96 +/- 0.84) ng/ml and (2.23 +/- 0.99) ng/ml in unstable angina and acute myocardial infarction group, respectively] than in stable coronary heart disease patients [(1.20 +/- 0.76) ng/ml, P < 0.05]. Serum sCD40L was significantly correlated with MMP-9 (r = 0.401 , P < 0.01), and sCD40L level was significantly correlated with TG (r = 0.254, P = 0.039), HDL (r = -0.234, P = 0.031), and HDL-C (r = -0.253, P = 0.024). CONCLUSION: Serum sCD40L and MMP-9 levels were elevated in acute coronary syndrome, suggesting the possible relation to the pathogenesis of ACS and it may serve as a potential marker of plaque stability.

Adult↗
PubMed2003

Atorvastatin reduces plasma MCP-1 in patients with acute coronary syndrome.

BACKGROUND: The monocyte chemoattractant protein-1 (MCP-1) is a chemokine responsible for the recruitment of monocytes to sites of inflammation. MCP-1 may play critical roles in plaque instability. Anti-inflammation may be one benefit of statin drugs in acute coronary syndrome (ACS). We investigated the effects of atorvastatin therapy on plasma MCP-1 concentrations and production of MCP-1 released by peripheral blood monocytes from ACS patients. METHODS: Forty patients with ACS were randomly separated into two groups, those receiving conventional therapy (Group A, n=20), and conventional therapy+atorvastatin (10 mg/day, Group B, n=20). The study the effects of atorvastatin on secretion and expression of MCP-1, human peripheral blood monocytes from healthy donors were incubated with atorvastatin (0.1-10 micromol/l) for up to 24 h in vitro. MCP-1 concentrations in plasma and monocytes culture supernatants were measured by enzyme-linked immunosorbent assays (ELISA). MCP-1 expression was measured by RT-PCR. RESULTS: Plasma concentrations of MCP-1 were significantly lower after 4 weeks therapy in both groups of patients [Group A from 97.4 (50.1-164) to 72.6 (36.3-156) pg/ml, Group B from 101 (60-178) to 45 (29-91) pg/ml, (P<0.05, respectively)]. Compared with conventional therapy alone, atorvastatin significantly further reduced plasma MCP-1 concentrations. There was no significant correlation between the degree of changes in plasma MCP-1 and LDL-C. In vitro, atorvastatin inhibits production of MCP-1 up to 73%, in a concentration-dependent manner, and suppressed MCP-1 expression in peripheral blood monocytes. CONCLUSIONS: Atorvastatin reduced plasma MCP-1 concentrations in patients with ACS. These effects may explain some clinical benefits of statins in the treatment of these patients.

Atorvastatin↗
PubMed2003

Atorvastatin reduces interleukin-6 plasma concentration and adipocyte secretion of hypercholesterolemic rabbits.

BACKGROUND: Interleukin-6 (IL-6) is secreted by adipocytes and may be involved in atherosclerosis. Few studies have assessed the influence of statins on IL-6 secretion in adipocytes. METHODS: Rabbits on high-cholesterol diets were randomly given either atorvastatin 1.5 mg/kg day(-1) (n=5) or starch (n=5) for 2 weeks. Subcutaneous adipose was collected for adipocytes culture. IL-6 concentrations in plasma and adipocytes culture supernatant were measured by ELISA. RT-PCR was used to evaluate peroxisome proliferator-activated receptor (PPAR) gamma mRNA expression. The in vitro effect of atorvastatin on IL-6 production in adipocytes was observed. RESULTS: Two weeks atorvastatin treatment resulted in significant reduction of circulating IL-6 concentrations, which was associated with IL-6 secretion in adipocytes (r=0.849, P<0.01). Meanwhile mRNA expression of PPARgamma in adipocytes was intimately related to the IL-6 secretion in adipocytes (r=-0.900, P<0.01). Atorvastatin induced the decreased IL-6 secretion in dose-dependent manner. CONCLUSIONS: Atorvastatin can inhibit IL-6 secretion in adipocytes possibly through upregulating PPARgamma, which may help to explain the anti-inflammatory effects of statins use.

Adipocytes↗
PubMed2003

[Changes in fatty acid composition of serum cholesteryl esters in patients with chronic heart failure].

OBJECTIVE: To investigate the changes in fatty acid composition of serum cholesteryl esters in patients with chronic heart failure (CHF). METHODS: The levels of serum TG, TC, HDL, and LDL in 36 patients with CHF and 20 healthy controls were measured and fatty acid cholesteryl esters were determined by high performance liquid chromatography. RESULTS: In the patients with CHF, the level of linoleic acid was significantly higher than that in the control group (P < 0.05), but the level of arachidonic acid was significantly lower than that in the control group (P < 0.05). The levels of TC, TG, HDL, and LDL were not significantly different between the two groups. CONCLUSION: Changes in fatty acid composition of serum cholesteryl esters exist in the patients with CHF.

Adult↗
PubMed2003

[Construction of double-subunit co-expression eukaryotic vector of human interleukin 12].

OBJECTIVE: To construct the double-subunit co-expression plasmid P(+)/IL-12 to fulfill the gene therapy. METHODS: The full length cDNAs of P40 and P35, two subunits of hIL12, were amplified from the reverse transcription production of human embryo kidney using polymerase chain reaction (PCR) and respectively cloned into eukaryotic expression vector pcDNA3.1(+/-) to construct the single-subunit plasmids--P(+)/P40 and P(-)/P35. Then we linked cDNAs of P40 and P35 tandem and cloned them into pcDNA3.1(+) to get P(+)/IL-12 plasmid. The hIL-12 protein in supernate was detected with enzyme-linked immunoabsorbent assay (ELISA) after P(+)/IL-12 was transfected into HepG2 through liposome. RESULTS: The plasmid of P(+)/IL-12 was testified using enzyme cutting and sequencing analysis. ELISA showed that hIL-12 protein could be expressed after transfecting into HepG2. CONCLUSION: The successful construction of P(+)/IL-12 plasmid can not only simplify the operation steps but also mimic hIL-12 physiological expression style in the gene therapy, thus laying the foundation for the use of hIL-12 in the gene therapy.

Escherichia coli↗
PubMed2003

[Ambulatory pulse pressure and left ventricular hypertrophy in patients with essential hypertension].

OBJECTIVE: To evaluate the relationship between the left ventricular hypertrophy (LVH) and the ambulatory pulse pressure and aortic root dimension (AOD) in essential hypertensive patients. METHODS: We monitored the 24-hour ambulatory blood pressure and applied echocardiography in 107 essential hypertensive patients. Using the left ventricular mass index (LVMI) as an index in evaluating LVH, the patients were divided into 2 groups: 29 cases in the LVH group and 78 in the non-LVH group. RESULTS: The average levels of 24-hour pulse pressure, daytime pulse pressure, nighttime pulse pressure and AOD were significantly different between patients with LVH and without LVH (P < 0.05). Multiple stepwise regression analysis showed that the changes in nighttime pulse pressure and AOD were closely related to LVMI (P < 0.001). CONCLUSION: The pulse pressure and AOD are important factors leading to LVH in patients with essential hypertension.

Adult↗
PubMed2003

[Apolipoprotein E gene expression in peripheral blood monocyte in children with obesity].

OBJECTIVE: Coronary heart disease (CHD) is one of the most common causes of death in the world. Some studies suggested that CHD begins in childhood. Obesity and dyslipidemia are important risk factors of coronary heart disease. Apolipoprotein (apo)E gene associated with dyslipidemia and coronary heart disease. The present study was designed to investigate the expression status of apoE gene in peripheral blood monocyte and association of apoE gene expression with lipids in children with obesity. METHODS: Among 32 children with obesity and 32 healthy children without obesity or overweight, ApoE gene expressions were determined by competitive reverse transcription-polymerase chain reaction in peripheral blood monocyte. The concentrations of plasma triglyceride, total cholesterol, low density lipoprotein-cholesterol, high density lipoprotein-cholesterol, lipoprotein(a), apoA I, apoB(100) and apoE were measured. RESULTS: Expression of apoE gene was detected in peripheral blood monocyte. Expression of apoE gene was significantly reduced in children with obesity as compared with control group (0.29 +/- 0.14 moles/mole GAPDH mRNA vs. 0.36 +/- 0.10 moles/mole GAPDH mRNA, t = 2.15, P < 0.05). The more severe was the degree of obesity, the more significantly reduced the expression of apoE gene; the degree of obesity was negatively correlated with the levels of expression of apoE gene (correlation coefficient = -0.40, P < 0.05). Compared with control group, the levels of triglyceride, total cholesterol, low density lipoprotein-cholesterol, and apoB(100) were higher, and those of high density lipoprotein-cholesterol, apoA I and apoE were lower in children with obesity [(1.68 +/- 0.50) mmol/L vs. (0.99 +/- 0.54) mmol/L, (4.47 +/- 0.91) mmol/L vs. (3.33 +/- 0.90) mmol/L, (2.23 +/- 0.71) mmol/L vs. (1.13 +/- 0.96) mmol/L, (94.48 +/- 9.97) mg/dl vs. (83.81 +/- 15.64) mg/dl, (1.47 +/- 0.39) mmol/L vs. (1.73 +/- 0.36) mmol/L, (112.71 +/- 27.86) mg/dl vs. (134.80 +/- 45.36) mg/dl, (24.50 +/- 10.92) mg/L vs.(35.07 +/- 9.79) mg/L, respectively, P < 0.05]. ApoE gene expression was associated with plasma lipids metabolism in children with obesity. The quantity of apoE gene expression was inversely associated with low density lipoprotein-cholesterol, positively correlated with apoE (correlation coefficient = -0.33, 0.35, respectively, P < 0.05). The quantity of apoE gene expression was not associated with total cholesterol, triglyceride, high density lipoprotein-cholesterol, lipoprotein(a), apoA I, and apoB(100) (correlation coefficient = -0.19, -0.11, 0.16, 0.09, 0.18, 0.22, P > 0.05). CONCLUSION: Expression of apoE gene was significantly reduced in peripheral blood monocyte in children with obesity. The quantity of apoE gene expression was associated with degree of obesity and abnormality of blood lipids.

Apolipoproteins E↗
PubMed2003

[Serum soluble CD40L level and its application in coronary heart disease].

OBJECTIVE: To investigate the serum level of soluble CD40 ligand (sCD40L) in coronary heart disease and its relationship with serum lipid levels. METHODS: Enzyme-linked immunosorbent (EIA) was used to measure sCD40L in 129 patients with coronary heart disease (46 with acute myocardial infarction, 37 with unstable angina pectoris and the other 46 with stable angina pectoris) and 30 matched healthy controls. RESULTS: sCD40L level was significantly higher in patients with acute coronary syndrome (ACS) [(2. 99 +/- 2.19), (2.23 +/- 0.67) ng/ml in acute myocardial infarction and unstable angina pectoris group, respectively] than that of those with stable coronary heart disease and that of controls [(1.12 +/- 0.42) and (0.89 +/- 0.55) ng/ml, respectively] (P < 0.05). Serum sCD40L level was significantly positively related to ApoB100 (r = 0.159, P = 0.046), and negatively related to HDL-C (r = -0.192, P = 0.015). CONCLUSION: The levels of sCD40L increase in acute coronary syndrome, which may be related to the pathogenesis of ACS, and can be used as a potential marker of plaque instability.

Angina Pectoris↗
PubMed2002

[Electrophoresis in the quantitative determination of cholesterol in lipoprotein fractions and its clinical application].

OBJECTIVE: To evaluate the clinical application of the electrophoresis method for measuring serum cholesterol in lipoproteins and to study the characteristics of lipoprotein fractions in patients with the acute coronary syndrome. METHODS: Cholesterol in lipoprotein fractions in fasting serum was measured by electrophoresis in 26 patients with the acute coronary syndrome and 20 patients with stable angina pectoris. The results were compared to cholesterol in lipoproteins measured with the regular method. RESULTS: There was a good correlation between the methods with coefficients of 0.922, 0.909, and 0.899 for LDL-C, HDL-C and VLDL-C, respectively. The serum levels of TG and VLDL-C in the patients with the acute coronary syndrome were significantly higher than those with stable angina pectoris [(0.47 +/- 0.33) mmol.L-1 vs. (0.29 +/- 0.19) mmol.L-1, P < 0.01, (1.82 +/- 0.70) mmol.L-1 vs. (1.31 +/- 0.48) mmol.L-1, P < 0.01]. CONCLUSION: The electrophoresis method for quantifying cholesterol in lipoprotein fractions is well correlated with the regular method. The serum levels of VLDL-C and TG in patients with the acute conronary syndrome are higher than those with stable angina.

Aged↗
PubMed2002

[Correlation between blood pressure variability and left ventricular hypertrophy in patients with primary hypertension].

OBJECTIVE: To study the correlation between blood pressure variability (BPV) and left ventricular hypertrophy (LVH) in patients with primary hypertension. METHODS: We monitored the 24-hour ambulatory blood pressure and determined the left ventricular mass index (LVMI) by two dimensional echocardiography in 87 patients with primary hypertension (PH) and 26 normal controls. RESULTS: The LVMI in the PH patients was significantly higher than that in the controls. It was positively correlated to the average level of the 24-hour systolic blood pressure (24 h-SBP), nighttime systolic blood pressure (n-SBP), and nighttime diastolic blood pressure (n-DBP) (r = 0.183, P < 0.05; r = 0.275, P < 0.01; r = 0.243, P < 0.05, respectively). It was also negatively correlated to the 24-hour systolic blood pressure variability (24 h-SBPV) and the daytime systolic blood pressure variability (d-SBPV) (r = -0.253, P < 0.01; r = -0.186, P < 0.05, respectively). The 24 h-SBPV in the patients with LVH was significantly lower than that of those without LVH, but there was no significant difference in d-SBPV and n-SBPV between the PH patients with LVH and those without LVH. CONCLUSION: The 24 h-SBPV is valuable in predicting LVH in hypertension.

Adult↗
PubMed2002

[Influence of postprandial hypertriglyceridemia on the endothelial function in elderly patients with coronary heart disease].

OBJECTIVE: To explore the changes of carotid atherosclerosis and the endothelial function after a high-fat meal in elderly patients with coronary artery disease (CAD). METHODS: The carotid intima-media thickness (IMTc) and the brachial artery flow-mediated vasodilation (FMD) before and after a high-fat meal were measured by the high-resolution ultrasound technique in 20 elderly patients with CAD and 22 healthy elderly subjects. RESULTS: The CAD patients had a higher IMTc (P < 0.01) and impaired FMD (P < 0.05) compared with the healthy subjects. The serum triglyceride level increased in the two groups after the meal. The CAD patients had a higher triglyceride peak response (TGPR) than the healthy subjects (P < 0.05). The IMTc of the two groups had no change before and after the meal. The postprandial FMD significantly aggravated in the two groups (P < 0.001); and the percent decrement of FMD in the CAD patients was obviously higher than that in the healthy subjects (P < 0.05). The postprandial TGPR was positively correlated with the fasting IMTc and the postprandial percent decrement of FMD (P < 0.01). CONCLUSION: The disordered postprandial metabolism of triglyceride-riched lipoproteins may play an atherogenic role by inducing endothelial dysfunction.

Aged↗
PubMed2002

[Congestive heart failure and paraoxonase].

OBJECTIVE: To determine the changes of paraoxonase activity in patients with heart failure. METHODS: The serum paraoxonase (PON) activity of the heart failure group and controls was measured with phenylacetate as the substrate. RESULTS: The serum PON activity of the heart failure patients significantly decreased as compared with the controls; after the treatment, the PON activity of heart failure was largely elevated; and the PON activity of the patients with heart failure was negatively correlated with tumor necrosis factor-alpha. CONCLUSION: The PON activity of patients with congestive heart failure significantly decreases.

Adult↗