血清趋化素水平与钙化性主动脉瓣狭窄程度的相关性研究

目的探讨血清趋化素(chemerin)水平在钙化性主动脉瓣狭窄(CAS)发病机制中的作用及与主动脉瓣狭窄程度的相关性。方法选取2016年11月至2019年11月于邯郸市第一医院心内科诊断为CAS的患者40例为CAS组,将CAS患者按主动脉瓣狭窄程度分为三组:轻度CAS组(n=14)、中度CAS组(n=15)及重度CAS组(n=11);另选取同期来院体检的无CAS的患者40例为对照组(年龄、性别与CAS组匹配)。采用酶联免疫吸附法(ELISA)测定各组血清chemerin水平;应用Spearman相关分析法评估chemerin和主动脉瓣狭窄程度的相关性。结果与对照组相比,CAS组患者的血清chemerin水平明显升高[(89.8±14.9)ng/ml vs.(60.1±21.3)ng/ml,P<0.05];三组不同狭窄程度CAS患者的血清chemerin水平较对照组均明显升高,差异有统计学意义(P<0.05),且随狭窄程度的加重,chemerin水平逐渐降低,其中轻度CAS组患者的chemerin水平最高;相关性分析显示,血清chemerin水平与主动脉瓣狭窄程度呈负相关性(r=-0.632,P<0.01)。结论血清chemerin水平与CAS狭窄程度有关,可作为辅助诊断CAS的血清炎症提示指标。     

代谢综合征患者血清hs-CRP、脂肪因子chemerin的变化及相关性研究

目的：：探讨代谢综合征患者血清高敏-C反应蛋白(hs-CRP)、脂肪因子chemerin的变化及其相关性。方法：选取收治的代谢综合征患者(代谢综合征组)及同期门诊体检正常健康者(对照组)各60例,进行体质量指数、腹围等基础指标检测,以免疫比浊法测定血清hs-CRP水平,酶联免疫吸附法测量血清chemerin水平。结果：代谢综合征组患者体质量指数、收缩压、舒张压、空腹血糖、甘油三酯及低密度脂蛋白均明显高于对照组(P<0.01或P<0.05);代谢综合征组患者血清hs-CRP、脂肪因子chemerin水平均明显高于对照组(P<0.01),代谢综合征组患者血清hs-CRP与脂肪因子chemerin水平间呈现正相关性(P<0.01)。结论：代谢综合征患者血清hs-CRP、脂肪因子chemerin水平明显高于正常人群,两种之间存在明显相关性。     

血清趋化素水平与代谢综合征的相关性研究

目的 探讨血清趋化素（Chemerin）水平与MS的相关性. 方法 选取非MS（Non-MS）组57例,MS组117例及健康对照（NC）组90名,按Chemerin水平从低到高分为Ter1、Ter2和Ter3亚组.所有研究对象行75 g OGTT和胰岛素释放试验,检测血脂、血清Chemerin、高敏C反应蛋白（hsC-RP）等相关生化指标. 结果 MS组血清Chemerin水平高于Non-MS组和NC组（P＜0.01）.从Ter1到Ter3亚组,BMI、WC、WHR、SBP、FPG、2 hPG、HbA1 c、FIns、HOMA-IR、TG、hsC-RP水平依次升高,HDL-C水平依次降低,MS的患病率依次增加（P＜0.05）.Chemerin与BMI、WC、WHR、SBP、FPG、2 hPG、HbA1 c、FIns、2 hIns、HOMA-IR、TG及hsC-RP呈正相关（P＜0.05）,与HDL-C、胰岛β细胞功能指数（HOMA-β）呈负相关（P＜0.01）.Logistic逐步回归分析显示,Chemerin是MS的独立危险因素（OR=2.197,P＜0.01）.受试者工作曲线（ROC）曲线提示Chemerin预测MS的界值为72.4 ng/ml.结论 Chemerin与MS的发生相关,可作为MS的独立预测指标之一.     

阻塞性睡眠呼吸暂停低通气综合征患者血清Chemerin、Apelin水平与胰岛素抵抗关系研究

目的探讨男性OSAHS患者血清Chemerin、Apelin水平与胰岛素抵抗的关系。方法选择0sAHS患者65例和健康对照组28例,分别采用酶联免疫吸附法测定所有研究对象血清Chemerin、Apelin水平,应用稳态模型评估胰岛素抵抗指数（HOMA-IR）。结果与对照组比较,OSAHS患者血清Chemerin、Apelin水平及HOMAIR均高于对照组（P值均〈0．05）。血清Chemerin和Apelin-12水平与AHI呈正相关（r=0．541和0．506,P〈0．01）,与LSaO2和MsaO2均呈负相关（r=-0．451,-0．401和-0．428,-0．385,P值均〈0．01）。血清Chemerin和Apelin-12水平与HOMA-1R呈正相关（r=0．438和0．375,P〈0．05）,血清Chemerin与血清Apelin-12水平两者呈正相关（r值=0．511,P〈0．01）。患者HOMA-IR变化与AHI、LSaO2、血清Chemerin和Apelin-12水平呈线性回归关系。结论OSAHS患者血清Chemerin、Apelin水平与胰岛素密切相关,同时与患者严重程度和低氧相关．     

Low dose aspirin is associated with plasma chemerin levels and may reduce adipose tissue inflammation

Chemerin is a peptide chemoattractant for macrophages and an adipokine regulating adipocyte differentiation and metabolism. Plasma chemerin is increased in chronic inflammatory diseases and in obesity. As inflammation and obesity are risk factors for coronary artery disease (CAD), we investigated possible associations of plasma chemerin with inflammatory markers and atherosclerosis in a CAD case–control study (n = 470). Chemerin levels were associated with C-reactive protein, BMI and LDL levels, and negatively associated with HDL levels. Mean plasma chemerin levels were similar in controls and CAD patients but significantly higher in CAD patients not taking low dose aspirin. To investigate the mechanism of chemerin reduction by aspirin, we analyzed chemerin expression in hepatocytes and adipocytes treated with aspirin in the presence and absence of inflammatory cytokines. Chemerin expression was upregulated by pro-inflammatory stimuli in adipocytes but not in hepatocytes. Treatment of stimulated hepatocytes and adipocytes with aspirin did not affect chemerin expression. However, treatment of inflammatory M1 macrophages with aspirin reduced secretion of the pro-inflammatory cytokines IL-1β and IL-6, and increased secretion of the anti-inflammatory IL-10. In summary, we show that plasma chemerin levels are associated with markers of inflammation and that they are significantly higher in CAD patients not treated with low dose aspirin. In addition, we show that low dose aspirin treatment reduces pro-inflammatory cytokine secretion by macrophages, which may lead to reduced chemerin secretion by adipocytes and may be a reason for the lower chemerin levels in the circulation of CAD patients on low dose aspirin.     

The Treponema pallidum outer membrane protein Tp92 activates endothelial cells via the chemerin/CMKLR1 pathway

Endothelium damage caused by Treponema pallidum is the key step in the systemic dissemination and pathophysiology of syphilis, particularly cardiovascular syphilis and neurosyphilis. However, the molecular mechanisms supporting endothelium damage of syphilis are undefined. The outer membrane proteins were thought to be involved. Tp92 was first identified as an outer membrane protein of T. pallidum. Homologous proteins to Tp92 play important roles in cell attachment, inflammation, and tissue destruction in other bacterial species. In this study, we investigated the effect of Tp92 on endothelial cells activation. The data showed that Tp92 induced chemerin production in activated endothelial cells. Endothelial cell-derived chemerin upregulated the expression of TNF-α and ICAM-1 in endothelial cells via CMKLR1. In addition, endothelial cell-derived chemerin promoted THP-1-derived macrophage migration towards endothelial cells. These findings suggest that Tp92 may play an important role in mediating endothelial cell activation by inducing the secretion of chemerin.     

血清趋化素及肿瘤坏死因子α水平与2型糖尿病肾脏病的相关性研究

目的观察不同分期糖尿病肾脏病(diabetic kidney disease,DKD)患者血清趋化素(chemerin)及肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)水平的变化,并探讨其与DKD的相关性。方法入选45名健康体检者作为正常对照(normal control,NC)组和133例2型糖尿病患者,后者根据尿微量白蛋白/肌酐(the value of urinary albumin/creatine ratio,ACR)水平分为单纯糖尿病(simple diabetes mellitus,SDM)组47例、微量白蛋白尿(micro albuminuria DKD,mic-DKD)组41例和大量白蛋白尿(macro albuminuria DKD,mac-DKD)组45例。采用ELISA法测定4组研究对象的血清chemerin和TNF-α水平,并分析DKD发生的危险因素。结果 NC组血清chemerin浓度为(34.14±7.54)ng/ml,TNF-α浓度为(103.99±20.43)ng/L。SDM组血清chemerin浓度为(38.23±5.48)ng/ml,TNF-α浓度为(134.42±27.31)ng/L。mic-DKD组血清chemerin浓度为(42.69±8.os)ng/ml,TNF-α浓度为(165.48±32.63)ng/L。mac-DKD组血清chemerin浓度为(47.32±9.11)ng/ml,TNF-α浓度为(227.53±58.31)ng/L。4组血清chemerin和TNF-α水平逐渐升高,组间比较差异具有统计学意义(均P0.05)。血清chemerin水平与TNF-α、超敏C反应蛋白(high sensitivity C-reactive protein,hs-CRP)、糖化血红蛋白(glycosylated hemoglobin,HbA1c)、血肌酐(SCr)及病程呈正相关,与高密度脂蛋白胆固醇(high-density lipoprotein cholesterol,HDL-C)呈负相关。血清TNF-α水平与尿ACR、HbA1c、hs-CRP、SCr、低密度脂蛋白胆固醇(ligh-density lipoprotein cholesterol,LDL-C)及病程呈正相关,与HDL-C呈负相关。Logistic回归分析显示,chemerin、TNF-α、白细胞、年龄、HbA1c、低HDL-C及高血压是DKD发生的独立危险因素。结论 Chemerin和TNF-α参与了DKD发病,检测其水平可以在一定程度上反映DKD病情的严重程度。     

Chemerin基因在自发性2型糖尿病大鼠脂肪组织中表达的研究

目的：研究网膜及皮下脂肪组织中Chemerin在自发性2型糖尿病OLETF大鼠中的基因表达水平,探讨Chemerin与肥胖、胰岛素抵抗及2型糖尿病发病关系的机制。方法：4周龄正常不出现糖尿病的LETO大鼠10只作为对照组,4周龄OLETF大鼠10只,2型糖尿病的OLETF大鼠9只,于42周时处死。取网膜及皮下脂肪组织,以实时荧光定量法检测网膜及皮下脂肪组织Chemerin基因的表达水平。皓果：模型组的网膜及皮下脂肪组织Chemerin的基因表达明显高于LETO对照组（P〈0．01）;模型组大鼠网膜脂肪组织Chemerin的基因表达明显高于皮下脂肪组织（P〈0．01）。结论：脂肪因子Chemerin基因表达水平的变化是肥胖、胰岛素抵抗和2型糖尿病发病的机制之一。     

初诊T2DM伴肥胖患者血浆Chemerin水平升高

目的:探讨初诊2型糖尿病(Type 2 diabetics,T2DM)伴肥胖患者血浆Chemerin水平变化及其与体重指数(Body mass index,BMI)、腰臀比(Waist hip ratio,WHR)、血脂、血糖、血浆胰岛素水平等的关系.方法:采用酶联免疫法测定了初诊T2DM非肥胖患者(Type 2 diabeics not with obesity,T2DM-nonob)、初诊T2DM伴肥胖患者(Type 2 diabetics with obesity,T2DM-ob)、正常糖耐量非肥胖者(Normal glucose tolerance not with obesity controls,NGT-nonob)和正常糖耐量肥胖者(Normal glucose tolerance with obesity controls,NGT-ob)血浆Chemerin水平,并分析了血浆Chemerin水平与BMI、WHR、血脂、血糖、血浆胰岛素、胰岛素抵抗指数(HOMA insulin resistance index,HOMA-IR)等的关系.结果:T2DM伴肥胖组血浆Chemerin水平明显高于T2DM不伴肥胖组和NGT不伴肥胖组[(73.3±9.5)μg/L vs(65.3±13.4)μg/L vs(58.5±19.5)μg/L,P<0.01和P<0.05)],NGT伴肥胖对照组血浆Chemerin水平明显高于NGT不伴肥胖对照组[(72.0±15.2)μg/L vs(58.5±19.5)μg/L,P<0.05];胰岛素抵抗组(Insulin resi-tance,IR)Chemerin水平明显高于胰岛素敏感组(Insulin sensitive,IS)[(70.7±9.6)μg/L vs(61.7±19.1)μg/L,P<0.01].多元回归分析结果表明WHR、体内脂肪百分比(Visceral fat %,FAT%)分别是影响血浆Chemerin水平的独立相关因素.结论:血浆Chemerin水平的改变与肥胖相关因素和胰岛素抵抗等有关,并可能参与了肥胖、胰岛素抵抗和T2DM的发生和发展.