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Objective To investigate the correlation between serum S100B level and ST-segment elevation myocardial infarction and its diagnostic significance. Methods A total of 546 patients admitted to the Department of Cardiology, General Hospital of Shenyang Command from Sep. 2016 to Jan. 2018 were recruited in present research, including control group (n=105), unstable angina pectoris (UAP) group (n=100), non ST-segment elevation myocardial infarction (NSTEMI) group (n=101) and ST-segment elevation myocardial infarction (STEMI) group (n=240). The serum S100B level was detected by enzyme-linked immunosorbent assay (ELISA), and the spearman correlation, multivariate logistic regression and receiver operating characteristic curve (ROC) were used to analyze the data. Results The serum S100B levels increased in turn as control group, UAP group, NSTEMI group and STEMI group with statistical differences among the four groups (P

Objective To investigate the correlation of chemokine CX3CL1 and the major adverse cardiovascular events (MACCE) within 1 year in patients with ST elevation myocardial infarction (STEMI). Methods Five hundred patients with STEMI were continuously selected from the Department of Emergency, General Hospital of Shenyang Command, and 5ml venous blood was extracted at the time of admission. Plasma CX3CL1 levels were detected by ELISA. The median of CX3CL1 plasma concentration of all selected patients (2108.3pg/ml) was used to assign the patients to low expression group (

Objective To investigate whether chemokine CC motif 2 (CCL2) is involved in the high residual platelet response, and the mechanism of CCL2 being involved in the regulation of platelets. Methods Forty patients with ST elevation myocardial infarction (STEMI) were admitted. P2Y12 reaction unit (PRU) was detected by VerifyNow. Forty patients were divided into high platelet reactivity group (high reactivity group, n=24) and normal platelet reactivity group (normal reactivity group, n=16) according to the results of PRU detection. Plasma CCL2 concentration of the STEMI patients was examined by ELISA. The expressions of CCL2 and CCR2 in the platelets were detected by Western blotting. After CCL2 stimulation, the kinases of which phosphorylation was changed in the platelets were screened by ARY003B protein chips. The phosphorylation of p38MAPK and HSP27 in the platelets was tested by Western blotting after CCL2 stimulation in the presence or absence of CCR2 antagonist (RS 102895) or p38MAPK signal pathway inhibitor (SB 203580). Results The plasma CCL2 concentration of high reactivity group was markedly higher than that of normal reactivity group. Moreover, compared with normal reactivity group, the expressions of CCL2 and CCR2 in the platelets of high reactivity group significantly increased. After the platelets were stimulated by CCL2, the phosphorylation of p38α and HSP27 enhanced in the platelets by protein chips screening. When RS 102895 or SB 203580 was treated before CCL2 stimulation, the phosphorylation of p38MAPK and HSP27 decreased. Conclusions CCL2 participates in high residual platelet response in an autocrine/paracrine way. CCL2/CCR2 might affect the function of platelets through p38MAPK- HSP27 signal pathway. DOI: 10.11855/j.issn.0577-7402.2017.05.09

Objective To observe the effects of miR-124 on the proliferation and apoptosis of endothelial cells of umbilical cord vein in order to explore the role of miR-124 in the pathogenesis of atherosclerosis. Methods The expression levels of miR124 in plasma of 40 patients with coronary heart disease and 40 healthy control participants were examined using quantitative RTPCR. CCK8 assay and BrdU incorporation assay were used to analyze the effects of miR-124 on the proliferation of human umbilical vein endothelial cells (HUVECs). The effect of miR-124 on HUVEC apoptosis was examined by TUNNEL staining. The effects of miR-124 on the expression of proapoptotic protein cleaved caspase 3 and anti-apoptotic protein Bcl-2 in HUVECs were examined by Western blotting. Results Compared with healthy controls, plasma miR-124 was down-regulated in patients with coronary artery disease. In vitro experiment, miR-124 significantly promoted HUVEC proliferation, and it also inhibited HUVECs apoptosis by affecting the expressions of cleaved caspase 3 and Bcl-2. Conclusions MiR-124 could promote the proliferation and inhibit the apoptosis of HUVECs. This may provide a theoretical basis for clarifying the mechanisms of atherosclerosis. DOI: 10.11855/j.issn.0577-7402.2016.01.02

Objective To investigate the effects of chemokine ligand 16 (CXCL16) in high salt induced myocardial remodeling in salt sensitive hypertensive rats. Methods Sixty-four Dahl salt sensitive (Dahl-SS) rats were randomly divided into normal salt (NS, 0.3% NaCl) and high salt (HS, 8.0% NaCl) group, 32 rats for each group. Blood pressure was measured by tail-cuff method every week. Hearts were harvested and the expression of CXCL16 in heart tissues was detected by Western blotting at the 2nd, 4th, 6th and 8th week after NS or HS feeding. Immunofluorescence double staining was used to detect the colocalization of CXCL16 with both cardiomyocytes and cardiac fibroblasts. Immunofluorescence and immunohistochemical staining were used to detect the expression of CXCL16 and the biomarker of macrophage in the myocardial tissue after 6 week and 8 week of NS or HS feeding. Myocardial fibrosis was evaluated by HE and Masson trichrome staining. Results Compared with that in NS group, the systolic pressure and diastolic pressure in HS group increased significantly after 1 week of HS feeding (147.10±3.67mmHg vs128.57±6.32mmHg, P

Objective To establish a metabolic syndrome model of C57BL/6 mice by high-salt and high-fat diet, and investigate the effects of angiotensin converting enzyme 2 (ACE 2) and angiotensin (1-7) on renal damage in mice. Methods Fifty-six male C57BL/6 mice were randomly divided into 7 groups (8 each), and fed with normal diet (0.3% NaCl, 10% fat), high-salt diet (8% NaCl, 10% fat), high-fat diet (0.3% NaCl, 60% fat), high-salt and high-fat diet (8% NaCl, 60% fat), high-salt and high-fat diet with enalapril 20mg/(kg•d), with valsartan 50mg/(kg•d), and with valsartan 50mg/(kg•d) plus Mas receptor antagonist (A-779) 150ng/(kg•d), respectively for 16 weeks. Basal metabolic index including blood pressure, body weight, blood glucose and urinary albumin excretion rate (UAER) were tested. After intraperitoneal anesthesia with chloral hydrate, the blood was collected from the carotid artery. Serum angiotensin Ⅱ and angiotensin (1-7) levels were detected by ELISA; Western blotting was performed to evaluate the expression of ACE 2 protein and collagen Ⅲ in renal tissue; renal pathological changes were observed by HE and Masson staining. Results The blood pressure, ratio of visceral fat weight/body weight, blood lipid, blood glucose and UAER increased significantly in the C57BL/6 mice fed with high-salt and high-fat diet for 16 weeks, and the renal fibrosis change was obvious, serum angiotensin Ⅱ level increased, expressions of ACE 2 and angiotensin (1-7) decreased significantly in the renal tissue. In different intervention groups, valsartan obviously alleviated the abnormal metabolism, ameliorated renal injury, promoted the expression of ACE2 and angiotensin (1-7) in the kidney and serum. However, no significant change was observed in the groups with intervention of enalapril or valsartan+A-779 compared with non-intervention group. Conclusions High-salt and high-fat diet can be used to successfully establish the model of metabolic syndrome in C57BL/6 mice. Valsartan, an angiotensin Ⅱ receptor blocker, can alleviate the metabolic abnormality caused by the high-salt and high-fat diet, and the protection mechanism may be related to up-regulation of angiotensin (1-7). DOI: 10.11855/j.issn.0577-7402.2013.10.001

Objective To explore the relationship between the polymorphism of CCR7 rs3136685 and the coronary artery disease (CAD) in Han population in north China. Methods A total of 578 cases (including 287 patients with CAD and 291 control individuals) admitted to General Hospital of Shenyang Military Command from Mar. 2010 to Dec. 2011 were enrolled in the present study. All the subjects were unrelated individuals of Chinese Han inhabited in the northeast area of China, and had undergone coronary angiography. Those with 50% or more angiostenosis in one or more coronary arteries were sorted out as CAD group, which were then divided in 3 subgroups: namely angiostenosis in one vessel (n=104), in two vessels (n=89) and in three vessels (n=94). Those with normal angiography and no evidence of atherosclerosis were grouped as controls. Genomic DNA was extracted from blood leukocytes and polymorphic genotypes were determined by polymerase chain reaction and sequencing analysis. The correlation of rs3136685 genotype and allele frequency to CAD and the angiographic severity of CAD were analyzed. Results Three genotypes (GG, AG and AA) were detected in CCR7 rs3136685 genetic locus, their frequencies were 42.9%, 45.6% and 11.5%, respectively, in CAD group; and 43.0%, 44.3% and 12.7%, respectively, in control group (P>0.05). The distribution of the 3 genotypes in the both groups was coincident with the law of equilibrium. The distribution frequencies of A allele in CAD group and control group were 34.3% and 34.9% respectively, with no significant difference (P>0.05). Further stratification analysis among the polymorphism of CCR7 rs3136685 and angiographic severity of CAD also yielded negative results (P>0.05). Conclusion The CCR7 rs3136685 polymorphism is unlikely to be a major contributor to the pathogenesis of CAD in Han population in north China.

Objective To investigate the correlation of the single nucleotide polymorphism (SNP) of PON1 (Paraoxonase-1) gene rs854572 to the occurrence of clopidogrel resistance (CR). Methods A case-control method was employed in present study. A total of 850 hospitalized patients with coronary artery diseases (CAD) in General Hospital of Shenyang Command were enrolled. The residual platelet aggregation rate (RPA) induced by 20μmol/L of adenosine diphosphate (ADP) was detected by optical nephelometry, and RPA≥70% was defined as CR. Accordingly, all the enrolled 850 patients were then divided into CR group (n=215) and non-CR (NCR) group (n=635). Polymerase chain reaction (PCR) and pyrophosphate sequencing were executed to determine the genotypes and the allele frequencies of PON1 gene rs854572. Results The genotype frequencies in rs854572 of PON1 gene conformed well to the Hardy-Weinberg equilibrium in both CR group and NCR group. Three frequencies of genotype CC, CG and GG were 23.7%, 49.3%, 27.0% in CR group, and 24.1%, 50.2%, 25.7% in NCR groups, respectively. No significant difference in genotype and allele frequency existed between CR group and NCR group (P=0.93 and 0.76, respectively). Logistic regression analysis revealed that no correlation between rs854572 SNP of PON1 gene and the formation of CR in patients with CAD after adjustment of correspondent factors including age, gender, body mess index, smoking, hypertension, diabetes mellitus and hyperlipidemia. Conclusions It is considered that no correlation exists between PON1 gene rs854572 polymorphism and clopidogrel resistance in patients with coronary heart disease.