Predictive values of sST2 and IL-33 for heart failure in patients with acute myocardial infarction

Timely prediction of the risk of heart failure in acute myocardial infarction patients is critical for better prognosis. This article aims to evaluate the predictive value of serum soluble growth stimulation expressed gene 2 (sST2) and interleukin-33 in patients with acute myocardial infarction complicated by heart failure. A total of 42 healthy controls and 144 acute myocardial infarction patients were recruited in the study. According to Killip cardiac function classification as the basis for concurrent heart failure, they were distributed into non-heart failure group (n = 76) and heart failure group (n = 68). ELISA was utilized to determine the serum sST2 and interleukin-33 levels, and the diagnostic efficiency was evaluated by receiver operating characteristics curve. sST2 and interleukin-33 levels in patients with acute myocardial infarction were significantly increased when compared with normal healthy controls, and were further enhanced in the heart failure group. With the increased Killip cardiac function classification, interleukin-33 and sST2 levels were gradually elevated. Multivariate analysis indicated that interleukin-33 and sST2 could be used as independent predictors for heart failure combined with acute myocardial infarction.     

血清Trx1、FGL2与急性心肌梗死后心力衰竭患者预后的关系

摘要 目的：探讨血清硫氧还蛋白1（Trx1）、纤维蛋白原样蛋白2（FGL2）与急性心肌梗死后心力衰竭患者预后的关系。方法：选择2019年10月至2020年5月我院收治的158例急性心肌梗死后心力衰竭患者作为观察组,并根据心功能Killip分级分为Ⅱ级组54例、Ⅲ级组57例、Ⅳ级组47例。另选择同期我院收治的102例急性心肌梗死患者作为对照组。入院后采用酶联免疫吸附法（ELISA）检测所有患者血清Trx1、FGL2水平;观察组患者出院后随访2年,并根据是否出现主要不良心血管事件（MACE）将患者分为预后不良组和预后良好组。采用多因素Logistic回归分析影响急性心肌梗死后心力衰竭患者预后的相关因素,采用受试者工作特征（ROC）曲线评估血清Trx1、FGL2对急性心肌梗死后心力衰竭患者预后的预测价值。结果：观察组血清FGL2水平明显高于对照组,血清Trx1水平明显低于对照组（P<0.05）;心功能Killip分级Ⅳ级组患者血清Trx1水平明显低于Ⅱ级组、Ⅲ级组（P<0.05）,血清FGL2水平明显高于Ⅱ级组、Ⅲ级组（P<0.05）。预后不良组患者血清Trx1、LVEF均明显低于预后良好组,而年龄、血清FGL2及血尿酸、血肌酐、N末端B型利钠肽原（NT-proBNP）均明显高于预后良好组（P<0.05）,两组心功能Killip分级比例比较差异有统计学意义（P<0.05）。多因素Logistic回归分析显示,年龄（较高）、心功能Killip分级为Ⅳ级、Trx1下降、FGL2升高均是影响急性心肌梗死后心力衰竭患者预后的危险因素（P<0.05）。ROC曲线结果显示,血清Trx1、FGL2预测急性心肌梗死后心力衰竭患者预后的曲线下面积分别为0.807、0.811,两者联合检测预测急性心肌梗死后心力衰竭患者预后的曲线下面积为0.889。结论：急性心肌梗死后心力衰竭患者血清中Trx1水平降低,FGL2水平升高,且血清Trx1、FGL2水平与患者心功能分级及预后密切相关,可作为评估急性心肌梗死后心力衰竭患者预后的辅助性指标。     

Osteopontin inhibits interleukin-1beta-stimulated increases in matrix metalloproteinase activity in adult rat cardiac fibroblasts: role of protein kinase C-zeta

We have shown that osteopontin (OPN), an extracellular matrix protein, plays an important role in post myocardial infarction (MI) remodeling by promoting collagen synthesis and accumulation. Interleukin-1beta (IL-1beta), increased in the heart following MI, increases matrix metalloproteinase (MMP) activity in cardiac fibroblasts in vitro. Here, we show that OPN alone has no effect on MMP activity or expression. However, it reduces IL-1beta-stimulated increases in MMP activity and expression in adult rat cardiac fibroblasts. Pretreatment with bovine serum albumin had no effect on MMP activity or protein content, whereas GRGDS (glycine-arginine-glycine-aspartic acid-serine)-pentapeptide (which interrupts binding of RGD-containing proteins to cell surface integrins) and monoclonal antibody m7E3 (a rat beta3 integrins antagonist) inhibited the effects of OPN. Inhibition of PKC using chelerythrine inhibited the activities of both MMP-2 and MMP-9. Stimulation of cells using IL-1beta increased phosphorylation and translocation of PKC to membrane fractions, which was inhibited by OPN. OPN inhibited IL-1beta-stimulated increases in translocation of PKC-zeta from cytosolic to membrane fractions. Furthermore, the levels of phospho-PKC-zeta were lower in the cytosolic fractions of OPN knock-out mice hearts as compared with wild type 6 days post-MI. Inhibition of PKC-zeta using PKC-zeta pseudosubstrate inhibited IL-1beta-stimulated increases in MMP-2 and MMP-9 activities. These observations suggest that OPN, acting via beta3 integrins, inhibits IL-1beta-stimulated increases in MMP-2 and MMP-9 activity, at least in part, via the involvement of PKC-zeta. Thus, OPN may play a key role in collagen deposition during myocardial remodeling following MI by modulating cytokine-stimulated MMP activity.     

Apela improves cardiac and renal function in mice with acute myocardial infarction

Apela was recently identified as a new ligand of the apelin peptide jejunum (APJ) receptor. The purpose of this study was to investigate the role of apela in post‐myocardial infarction (post‐MI) recovery from cardiorenal damage. A murine MI model was established, and apela was then infused subcutaneously for two weeks. Echocardiographs were performed before and after infarction at the indicated times. Renal function was evaluated by serum and urine biochemistry. Immunohistochemistry of heart and kidney tissue was performed by in situ terminal deoxynucleotidyl transferase‐mediated dUPT nick end‐labelling reaction. Compared to the control group (MI/vehicle), the average value of the left ventricular ejection fraction in apela‐treated mice increased by 32% and 39% at 2‐ and 4‐week post‐MI, respectively. The mean levels of serum blood urea nitrogen,creatinine, N‐terminal pro‐brain natriuretic peptide and 24‐hour urine protein were significantly decreased at 4‐week post‐MI in apela‐treated mice relative to that of control animals. At the cellular level, we found that apela treatment significantly reduced myocardial fibrosis and cellular apoptosis in heart and kidney tissue. These data suggest that apela improves cardiac and renal function in mice with acute MI. The peptide may be potential therapeutic agent for heart failure.     

Targeted deletion of MMP-2 attenuates early LV rupture and late remodeling after experimental myocardial infarction

Matrix metalloproteinase-2 (MMP-2) is prominently overexpressed both after myocardial infarction (MI) and in heart failure. However, its pathophysiological significance in these conditions is still unclear. We thus examined the effects of targeted deletion of MMP-2 on post-MI left ventricular (LV) remodeling and failure. Anterior MI was produced in 10- to 12-wk-old male MMP-2 knockout (KO) and sibling wild-type (WT) mice by ligating the left coronary artery. By day 28, MI resulted in a significant increase in mortality in association with LV cavity dilatation and dysfunction. The MMP-2 KO mice had a significantly better survival rate than WT mice (56% vs. 85%, P < 0.05), despite a comparable infarct size (50 +/- 3% vs. 51 +/- 3%, P = not significant), heart rate, and arterial blood pressure. The KO mice had a significantly lower incidence of LV rupture (10% vs. 39%, P < 0.05), which occurred within 7 days of MI. The KO mice exerted less LV cavity dilatation and improved fractional shortening after MI by echocardiography. The LV zymographic MMP-2 level significantly increased in WT mice after coronary artery ligation; however, this was completely prevented in KO mice. In contrast, the increase in the LV zymographic MMP-9 level after MI was similar between KO and WT mice. MMP-2 activation is therefore considered to contribute to an early cardiac rupture as well as late LV remodeling after MI. The inhibition of MMP-2 activation may therefore be a potentially useful therapeutic strategy to manage post-MI hearts.     

老年冠心病患者血清Lp-PLA2、hs-CRP、IL-27及MMP-9水平与Gensini积分的相关性研究*

目的:探讨老年冠心病患者血清脂蛋白相关磷脂酶A2(Lp-PLA2)、高敏C反应蛋白(hs-CRP)、白细胞介素-27(IL-27)及基质金属蛋白酶-9(MMP-9)水平与Gensini积分的相关性。方法:选取2015年10月至2018年2月我院收治的冠心病患者142例为研究对象,将所有患者按照不同的冠心病类型分为不稳定型心绞痛(UAP)组54例、稳定型心绞痛(SAP)组40例和急性心肌梗死(AMI)组48例。同时根据患者Gensini积分将其分为轻度47例、中度51例和重度44例。比较不同冠心病类型、不同严重程度的Lp-PLA2、hs-CRP、IL-27、MMP-9水平及Gensini积分,并分析冠心病患者上述指标水平与Gensini积分的相关性。结果:AMI组患者Lp-PLA2、hs-CRP、IL-27、MMP-9水平及Gensini积分均高于UAP组和SAP组,且UAP组高于SAP组(P0.05)。重度患者Lp-PLA2、hs-CRP、IL-27、MMP-9水平及Gensini积分均高于中度和轻度患者,且中度患者高于轻度患者(P0.05)。经Spearman相关性分析结果显示,冠心病患者Lp-PLA2、hs-CRP、IL-27、MMP-9水平与Gensini积分均呈正相关(P0.05)。结论:老年冠心病患者Lp-PLA2、hs-CRP、IL-27及MMP-9水平与患者冠状动脉病变Gensini积分均呈正相关。临床根据Lp-PLA2、hs-CRP、IL-27及MMP-9水平的变化,有助于评估老年冠心病患者的病情严重程度。     

急性心肌梗死患者肠道优势菌群分析

目的探讨急性心肌梗死患者肠道优势菌群的改变及其与疾病严重程度的关系。方法共筛选急性心肌梗死患者71名及正常健康体检者33名,急性心肌梗死患者根据是否心衰分为急性心肌梗死组36名和急性心肌梗死伴泵衰竭组35名,所有入选者收集大便及血清标本,分别采用qPCR及化学发光仪测定肠道优势菌群改变和血清脑钠肽前体及肌钙蛋白水平。结果急性心肌梗死患者肠道优势菌群显著改变,肠道肠杆菌以及肠球菌细菌数量较对照组显著增加,均与脑钠肽前体、肌钙蛋白、Killip分级显著正相关,而双歧杆菌、乳酸杆菌等细菌数量显著降低,与脑钠肽前体、肌钙蛋白、Killip分级显著负相关。结论急性心肌梗死患者呈现典型的肠道菌群紊乱,且与患者疾病严重程度相关。     

Matrix metalloproteinase expression in cardiac myocytes following myocardial infarction in the rabbit

Myocardial infarction (MI), leads to cardiac remodeling, thinning of the ventricle wall, ventricular dilation, and heart failure, and is a leading cause of death. Interactions between the contractile elements of the cardiac myocytes and the extracellular matrix (ECM) help maintain myocyte alignment required for the structural and functional integrity of the heart. Following MI, reorganization of the ECM and the myocytes occurs, contributing to loss of heart function. In certain pathological circumstances, the ECM is modulated such that the structure of the tissue becomes damaged. The matrix metalloproteinases (MMPs) are a family of enzymes that degrade molecules of the ECM. The present experiments were performed to define the time-course, isozyme subtypes, and cellular source of increased MMP expression that occurs following MI in an experimental rabbit model. Heart tissue samples from infarcted and sham animals were analyzed over a time-course of 1-14 days. By zymography, it was demonstrated that, unlike the sham controls, MMP-9 expression was induced within 24 hours following MI. MMP-3 expression, also absent in sham controls, was induced 2 days after MI. MMP-2 expression was detected in both the sham and infarcted samples and was modestly up-regulated following MI. Tissue inhibitor of metalloproteinase-1 (TIMP-1) expression was evaluated and shown to be down-regulated following MI, inverse of MMP-9 and MMP-3 expression. Further, MMP-9 and MMP-3 expression was detected by immunohistochemistry in myocytes within the infarct. Additional studies were conducted in which cultured rat cardiac myocytes were exposed to a hypoxic environment (2% O2) for 24 hours and the media analyzed for MMP expression. MMP-9 and MMP-3 were induced following exposure to hypoxia. It is speculated that the net increase in proteolytic activity by myocytes is a contributing factor leading to myocyte misalignment and slippage. Additional studies with a MMP inhibitor would elucidate this hypothesis.     

Serum apoproteins A and B and the lecithin: cholesterol acyl transferase activities in liver cirrhosis and hepatic coma patients

Serum apoproteins A and B and LCAT activities were estimated in 80 patients, 46 with posthepatic cirrhosis and 34 with alcoholic cirrhosis. The cirrhosis patients were also divided into compensated, decompensated, and hepatic coma subgroups. Apo-A and LCAT activities were significantly decreased in both cirrhotic groups without any significant difference between posthepatitic and alcoholic cirrhotic groups, while Apo-B was decreased in hepatic coma patients only. The decompensated cirrhosis patients showed lower Apo-A levels than the compensated cirrhosis patients and hepatic coma patients showed still lower levels compared to decompensated subgroup, while no significant decrease was observed in LCAT activities between compensated and decompensated cirrhosis patients. Apo-A level was correlated more significantly with serum albumin level than the LCAT activity. The study confirms that Apo-A level is highly related to the degree of liver injury and also suggests that this decrease may be mainly due to impaired liver synthesis and that the serum levels of Apo-A and Apo-B can be utilized in the differential diagnosis of chronic liver diseases.     

Serum MMP-8: A Novel Indicator of Left Ventricular Remodeling and Cardiac Outcome in Patients after Acute Myocardial Infarction

Objective

Left ventricular (LV) remodeling following myocardial infarction (MI) is characterized by progressive alterations of structure and function, named LV remodeling. Although several risk factors such as infarct size have been identified, LV remodeling remains difficult to predict in clinical practice. Changes within the extracellular matrix, involving matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs), are an integral part of left ventricular (LV) remodeling after myocardial infarction (MI). We investigated the temporal profile of circulating MMPs and TIMPs and their relations with LV remodeling at 1 year and clinical outcome at 3 years in post-MI patients.

Methods

This prospective multicentre study included 246 patients with a first anterior MI. Serial echocardiographic studies were performed at hospital discharge, 3 months, and 1 year after MI, and analysed at a core laboratory. LV remodeling was defined as the percent change in LV end-diastolic volume (EDV) from baseline to 1 year. Serum samples were obtained at hospital discharge, 1, 3, and 12 months. Multiplex technology was used for analysis of MMP-1, -2, -3, -8, -9, -13, and TIMP-1, -2, -3, -4 serum levels.

Results

Baseline levels of MMP-8 and MMP-9 were positively associated with changes in LVEDV (P = 0.01 and 0.02, respectively). When adjusted for major baseline characteristics, MMP-8 levels remained an independent predictor LV remodeling (P = 0.025). By univariate analysis, there were positive relations between cardiovascular death or hospitalization for heart failure during the 3-year follow-up and the baseline levels of MMP-2 (P = 0.03), MMP-8 (P = 0.002), and MMP-9 (P = 0.03). By multivariate analysis, MMP-8 was the only MMP remaining significantly associated with clinical outcome (P = 0.02).

Conclusion

Baseline serum MMP-8 is a significant predictor of LV remodeling and cardiovascular outcome after MI and may help to improve risk stratification.     

Prolonged activation of tumor necrosis factor (TNF)-alpha and its soluble receptors in chronic heart failure patients both in the compensated and decompensated state. Interplay between their levels and metalloproteinase-3

INTRODUCTION: Recent clinical and experimental studies indicate that upregulation of the TNF system can contribute to the progression of cardiac remodeling and heart failure decompensation, by promoting alterations in cardiomyocyte biology and extracellular matrix metabolism. Extracellular matrix turnover is regulated by the matrix metalloproteinases (MMPs), which are endogenous enzymes responsible for extracellular collagen degradation. The present study investigates the fluctuation of serum levels of TNF-alpha, soluble TNF receptor-1 (sTNFR1) and -2 (sTNFR2), in patients with chronic heart failure both during acute decompensation and the stable state of the syndrome. The second goal of this study was to determine if a relationship exists between serum MMPs profiles (MMP-1, MMP-2, MMP-3) and circulating TNF-alpha or its soluble receptors. METHODS: Our patient group consisted of 52 patients with chronic heart failure (NYHA III-IV; mean age: 65 +/- 4 years; hypertensive cardiomyopathy: 20, ischemic cardiomyopathy: 17, dilated cardiomyopathy: 10, valvular disease: 5), who were hospitalized for acute decompensation of the syndrome. Our control group consisted of 30 healthy subjects (mean age: 57 +/- 6 years). Serum levels of TNF-alpha, sTNFR1, sTNFR2 and MMP-1,-2,-3 were measured in heart failure patients by ELISA at admission and after one month as follow-up. Values are expressed as medians and interquartile ranges. RESULTS: In our patient group, we observed a statistically significant increase in the levels of sTNFR1 and sTNFR2 at admission (sTNFR1: 5.15 ng\mL, 4.49-8.90 ng\mL, P < 0.001, sTNFR2: 13.40 ng\mL, 6.10-21.50 ng\mL, P < 0.001), and at one-month follow-up (sTNFR1: 5.30 ng\mL, 4.61-6.90 ng\mL, P < 0.001, sTNFR2: 21.80 ng\mL, 11.50-25.20 ng\mL, P < 0.001), compared to the control group (sTNFR1: 3.83 ng\mL, 3.70-3.95 ng\mL, sTNFR2: 4.00 ng\mL, 3.40-5.40 ng\mL). There was a statistically significant difference in the levels of sTNFR2 between admission and follow-up (P < 0.05). Significant correlations between serum MMP-3 and sTNFR2 levels both at admission and follow up (r -/+ 0.460, P -/+ 0.005 and r -/+ 0.338, P -/+ 0.044, respectively) were also found. CONCLUSIONS: Soluble TNF receptors are elevated in heart failure patients both in acute decompensation and stable phase. We have detected higher levels of soluble TNFR2 during the compensated phase of heart failure, suggesting that TNFR2 receptors appear to stabilize the cytokine and thereby prolong its half-life and biological functions. Finally, TNF system-mediated cardiac remodeling may exist through the activation of MMP-3 signaling pathways.     

参附注射液联合新活素对老年慢性心力衰竭患者心功能及血清BNP、MMP-9、CypA水平的影响

目的:研究参附注射液联合新活素对老年慢性心力衰竭患者心功能及血清B型利钠肽(Brain natriuretic peptide,BNP)、基质金属蛋白酶-9(matrix metalloprotein-9,MMP-9)、亲环素(cyclophilin,CypA)水平的影响。方法:选择2015年6月至2017年5月在我院进行治疗的慢性心力衰竭患者100例,根据治疗方案不同分为观察组和对照组,对照组给予新活素治疗,观察组以对照组为基础联合参附注射液治疗。治疗后,观察和比较两组的临床疗效、不良反应的发生情况及治疗前后血清BNP、MMP-9、CypA、SCr和BUN水平、LVEF、SV、LVEDD的变化。结果:观察组总有效率显著高于对照组(P0.05),治疗后,观察组血清BNP、MMP-9、CypA、SCr、BUN、LVEDD水平及不良反应发生率均显著低于对照组(P0.05),LVEF、SV均明显高于对照组(P0.05)。结论:参附注射液联合新活素治疗慢性心力衰竭可有效改善患者心功能,降低血清BNP、MMP-9、CypA水平,提高临床疗效,减少不良反应。     

前列地尔对脑梗死患者血清MMP-9影响的大样本研究

目的:探讨前列地尔对脑梗死患者临床疗效和血清基质金属蛋白-9(MMP-9)水平影响。方法:选取南京军区福州总院,福建医科大学附属医院脑梗死患者480例,根据是否应用前列地尔注射液随机分为对照组(240例)和实验组(240例):比较两组患者治疗临床疗效和NIHSS、BI评分及血清MMP-9水平。结果:1实验组总有效率(94.17%)明显高于对照组(80.83%),P0.05;2患者的MMP-9水平均降低,与对照组比较,实验组降低明显,P0.05,以上差异均有统计学意义。3急性脑梗死患者血清中MMP-9水平与NIHSS值呈正相关,与BI评分值呈负相关。结论:前列地尔能够明显降低MMP-9水平,改善神经症状,改善NIHSS、BI评分,具有较大的临床意义。     

Selective spatiotemporal induction of matrix metalloproteinase-2 and matrix metalloproteinase-9 transcription after myocardial infarction

Myocardial remodeling after myocardial infarction (MI) is associated with increased levels of the matrix metalloproteinases (MMPs). Levels of two MMP species, MMP-2 and MMP-9, are increased after MI, and transgenic deletion of these MMPs attenuates post-MI left ventricular (LV) remodeling. This study characterized the spatiotemporal patterns of gene promoter induction for MMP-2 and MMP-9 after MI. MI was induced in transgenic mice in which the MMP-2 or MMP-9 promoter sequence was fused to the beta-galactosidase reporter, and reporter level was assayed up to 28 days after MI. Myocardial localization with respect to cellular sources of MMP-2 and MMP-9 promoter induction was examined. After MI, LV diameter increased by 70% (P < 0.05), consistent with LV remodeling. beta-Galactosidase staining in MMP-2 reporter mice was increased by 1 day after MI and increased further to 64 +/- 6% of LV epicardial area by 7 days after MI (P < 0.05). MMP-2 promoter activation occurred in fibroblasts and myofibroblasts in the MI region. In MMP-9 reporter mice, promoter induction was detected after 3 days and peaked at 7 days after MI (53 +/- 6%, P < 0.05) and was colocalized with inflammatory cells at the peri-infarct region. Although MMP-2 promoter activation was similarly distributed in the MI and border regions, activation of the MMP-9 promoter was highest at the border between the MI and remote regions. These unique findings visually demonstrated that activation of the MMP-2 and MMP-9 gene promoters occurs in a distinct spatial relation with reference to the MI region and changes in a characteristic time-dependent manner after MI.     

Overexpression of MMP-9 and Its Inhibitors in Blood Mononuclear Cells after Myocardial Infarction - Is It Associated with Depressive Symptomatology?

Background

Matrix metalloproteinase (MMP)-9 may play a central role in the development and progression of atherosclerosis. Emerging evidence also indicates an association between MMP-9 and depressive symptomatology. Here, we investigated whether expression of MMP-9 and its inhibitors in blood mononuclear cells and plasma were related to depressive symptoms in patients with a recent myocardial infarction (MI).

Methods and Results

Blood sampling was performed between 6 and 18 months after MI in 57 patients. Forty-one clinically healthy subjects were included as controls. Gene expression of MMP-9 and its main tissue inhibitors TIMP-1 and -2 were analyzed in freshly isolated or cultured blood mononuclear cells. Corresponding protein levels were assessed in cell supernatants and plasma. In post-MI patients, mRNA levels of MMP-9 and TIMP-1 and -2 were significantly higher than in controls while protein levels in cell supernatants and plasma did not differ between groups. The Center for Epidemiological Studies - Depression (CES-D) scale was used to assess depressive symptomatology. Repeated assessments during the first 18 months after MI showed significantly higher CES-D scores in patients compared with controls. However, there were no relationships between depressive mood and any of the measurements of MMP-9 or TIMPs.

Conclusion

Our findings indicate that overexpression of MMP-9 and TIMPs in blood mononuclear cells and elevated depressive symptoms represent two unrelated phenomena after MI.     

脑梗死患者内脂素和基质金属蛋白酶-9与颈动脉粥样硬化斑块易损性的关系

目的：探讨血清内脂素（Visfatin）72．基质金属蛋白酶-9（MMP-9）水平与脑梗死患者颈动脉粥样硬化王囊￡块稳定性的关系和血清visfatin和MMP-9的相关性。方法：选择脑梗死患者70例,根据颈动脉粥样硬化斑块性质分为易损性斑块组（n=43）和非易损性斑块组（n=27）,选取健康体检者30例作为对照组。测定血清Visfatin和MMP-9水平,并对二者间关系进行相关分析。结果：脑梗死伴颈动脉硬化组血清Visfatin、MMP-9水平高于正常对照组（P〈0．01）;易损性斑块组血清Visfatin和MMP．9水平高于非易损性斑块组,差异有统计学意义（P〈0．017）。外周血中的Visfatin水平与MMP-9呈正相关关系（r=0．643,P=0．000）。结论：在脑梗死患者中,血清Visfatin和MMP-9参与了颈动脉粥样硬化的病理生理过程,Visfatin和MMP-9升高可能与颈动脉粥样硬化斑块不稳定性的形成相关,Visfatin可通过调控MMP一9的分泌和活性从而改变斑块的易损性。     

依达拉奉联合疏血通对急性脑梗死患者的临床疗效及机制研究

目的:探讨依达拉奉联合疏血通对急性脑梗死患者的临床疗效及其可能作用机制。方法:收集我院治疗的80例急性脑梗死患者,随机分为实验组和对照组,每组40例。对照组患者给予依达拉奉注射液30 mg+生理盐水100 mg静脉滴注,2次/d;实验组患者在对照组基础上给予疏血通注射液6 g+生理盐水250 m L静脉滴注,2次/d,14 d为1个疗程。治疗后,对两组患者的血清血清基质金属蛋白酶-9(MMP-9),血管内皮生长因子(VEGF)、NIHSS以及临床疗效进行检测并比较。结果:与治疗前相比,两组患者治疗后血清MMP-9、VEGF水平以及NIHSS评分均显著下降(P0.05);与对照组相比,实验组患者治疗后血清MMP-9、VEGF水平以及NIHSS评分均较低(P0.05),且治疗总有效率较高(P0.05)。结论:依达拉奉联合疏血通能够有效提高急性脑梗死患者的临床疗效,改善神经功能缺损,这可能与其降低患者血清基质金属蛋白酶-9(MMP-9)及血管内皮生长因子(VEGF)水平有关。     

C - 反应蛋白在不同程度急性心梗患者中的相关性研究

目的:探讨C-反应蛋白(CRP)在急性心肌梗死患者中的变化及与心功能之间的关系。方法:选取121例急性心肌梗死(AMI)患者和50例健康对照者,酶联免疫吸附法(ELISA)检测血清C-反应蛋白(CRP)和B型钠尿肽(BNP)。结果:AMI患者血清CRP显著高于健康对照,AMI伴心功能III,IV级者血清BNP、CRP显著高于AMI伴心功能I,II级者。结论:血清CRP对于急性心肌梗死患者的心功能重要参考指标。     

血栓通联合依达拉奉对老年急性脑梗死患者氧化低密度脂蛋白和MMPs水平的影响及临床疗效

目的:探讨血栓通联合依达拉奉对老年急性脑梗死患者氧化低密度脂蛋白及MMPs水平的影响及临床疗效。方法:收集我院收治的126例急性脑梗死患者,随机分为实验组和对照组,每组各63例。对照组患者给予血栓通注射液治疗;实验组患者在对照组基础上给予依达拉奉治疗。观察并比较两组患者治疗前后血清氧化低密度脂蛋白(Ox-LDL)、基质金属蛋白酶2(MMP-2)及基质金属蛋白酶9(MMP-9)水平的变化情况以及临床疗效。结果:与治疗前相比,治疗后两组患者Ox-LDL,MMP-2及MMP-9水平均下降,差异具有统计学意义(P0.05);与对照组相比,实验组患者Ox-LDL,MMP-2及MMP-9水平较低,差异具有统计学意义(P0.05);与对照组相比,实验组患者的临床疗效较高,差异具有统计学意义(P0.05)。结论:血栓通联合依达拉奉能够降低老年急性脑梗死患者氧化低密度脂蛋白(Ox-LDL)、基质金属蛋白酶2(MMP-2)以及基质金属蛋白酶9(MMP-9)水平,临床疗效较好。     

Association of MMP-2 and MMP-9 with clinical outcome of neurocysticercosis

Matrix metalloproteinases (MMPs) are the major endopeptidases involved in proteolysis of blood brain barrier (BBB) during central nervous system (CNS) infections. The present study detected serum levels and activities of MMP-2 and MMP-9 in patients with neurocysticercosis (NCC) and their association with symptomatic disease. In total, 68 individuals with NCC (36 symptomatic patients with active seizures and 32 asymptomatic individuals) and 37 healthy controls were enrolled for the study. Serum MMP-2 and MMP-9 levels and their activities were measured by ELISA and gel zymography respectively. Mean serum MMP-2 levels (ng/ml) were higher both in asymptomatic and symptomatic NCC cases compared to healthy controls. However, significantly higher levels of serum MMP-9 (ng/ml) were detected only in symptomatic NCC patients compared to asymptomatic NCC cases and healthy controls. Levels of both MMPs positively correlated with symptomatic NCC. Serum MMP-2 activities were significantly higher in symptomatic and asymptomatic NCC compared to healthy controls whereas serum MMP-9 activity was significantly associated with symptomatic NCC compared to healthy controls and asymptomatic NCC. In conclusion, the elevated level of MMP-9 in serum appears to play an important role in the development of symptoms i.e. active seizures in patients with NCC. However, further studies are needed to elucidate its precise role in disease pathogenesis.