孕中期血清载脂蛋白CⅢ、Apelin、Chemerin水平及对妊娠期糖尿病诊断和不良妊娠结局的影响

目的观察孕中期血清载脂蛋白CⅢ(apo CⅢ)、Apelin、Chemerin水平,并探讨三者对妊娠期糖尿病(GDM)的诊断价值及与妊娠不良结局的关系。方法选取2017年8月—2019年8月经筛查确诊为GDM的87例孕妇作为观察组,另选取同期筛查正常的孕妇80例作为对照组。比较两组血清apo CⅢ、Apelin、Chemerin水平,三者之间的相关性采用Pearson相关分析;受试者工作特征(ROC)曲线分析三者对GDM的诊断价值;影响GDM不良妊娠结局的危险因素采用多因素Logistic回归分析。结果观察组血清apo CⅢ、Apelin、Chemerin水平均高于对照组(P<0.01)。血清apo CⅢ、Apelin、Chemerin之间均呈正相关性(P<0.01)。血清apo CⅢ、Apelin、Chemerin及三者联合诊断GDM的ROC曲线下面积分别为0.841、0.718、0.785及0.861,三者联合诊断的敏感度为63.2%,特异度为93.7%。不良妊娠结局GDM患者血清apo CⅢ、Apelin、Chemerin水平均高于正常妊娠结局GDM患者(P<0.05);孕中期血清apo CⅢ、Apelin、Chemerin水平升高均是影响GDM患者不良妊娠结局的独立危险因素(P<0.05,P<0.01)。结论孕中期GDM血清apo CⅢ、Apelin、Chemerin均呈高表达,三者联合对GDM具有较高的诊断价值,且是影响GDM患者不良妊娠结局的独立危险因素。     

Apelin/APJ系统与血管发生

Apelin/APJ系统是一种新型G蛋白偶联受体系统，在人与动物的多种组织中广泛表达。Apelin/APJ系统可影响哺乳动物的许多生物学特性，包括神经内分泌系统、心血管系统等。血管发生是指在已有血管的基础上依赖于内皮细胞，以出芽方式增殖、迁移并相互联结形成血管内膜腔，最终形成新血管的过程。血管发生在血管生理和病理条件下发挥着重要的作用，文章就近年来　Apelin在血管发生研究方面所取得的进展做一综述。     

Apelin及其受体和一氧化氮合酶在氧诱导的新生小鼠增生性视网膜病变中表达上调

 目的：通过观察apelin及其受体APJ和一氧化氮合酶（NOS）在氧诱导的新生小鼠增生性视网膜病变中的表达,探讨apelin/APJ和一氧化氮(NO)是否参与了早产儿视网膜病变新生血管的发生。方法：36只7日龄C57BL/6J新生小鼠随机均分为高氧组和对照组。高氧组暴露在75%±2%的氧浓度下5 d后,在正常空气环境下饲养5 d;对照组小鼠在正常氧环境下饲养10 d。两组均在17日龄处死,取左眼眼球做石蜡切片,HE染色计数突破内界膜的血管内皮细胞核数,以判断造模是否成功。实时荧光定量PCR检测右眼视网膜组织apelin和APJ mRNA的表达,免疫荧光组织化学法检测视网膜apelin、APJ、eNOS和iNOS蛋白的表达。结果：高氧组视网膜平均每个切面突破内界膜的血管内皮细胞核数(35.13±10.13)明显高于对照组(0.30±0.21,P<0.01）,说明造模成功。高氧组apelin和APJ mRNA水平显著高于对照组,分别为对照组的32.2倍和17.6倍（均P<0.01）。组织免疫荧光结果显示高氧组apelin和APJ蛋白表达明显强于对照组,并且主要强表达于新生血管周围;高氧组eNOS和iNOS蛋白表达明显强于对照组,但主要强表达于新生血管下方视网膜组织,在突破内界膜的血管内皮细胞核周围未见表达明显增强。结论：Apelin/APJ及NOS可能与氧诱导的新生小鼠增生性视网膜病变新生血管的发生有关。     

Apelin 调控心脏电生理特性的研究

Apelin是血管紧张素Ⅱ1型受体相关蛋白（APJ）的内源性配体,是由心肌细胞、血管内皮细胞、平滑肌细胞等合成一种血管内皮源性肽,广泛参与高血压、冠心病、心力衰竭、房颤等心血管疾病的发生发展过程。心肌细胞的电活动是心脏工作的基础,Apelin可通过调控Na＋、K＋和Ca2＋离子通道而增加心肌细胞兴奋性和传导性,改变心脏的电生理功能。本文将针对Apelin对心肌细胞的电生理特性的调控作以综述。     

老年高血压伴心力衰竭患者血浆Apelin水平的研究分析

目的比较高血压伴心力衰竭患者和单纯高血压患者血浆Apelin水平的差异。方法选取130例原发性高血压患者,根据是否有心力衰竭分为高血压伴心力衰竭组86例和单纯高血压组44例,检测2组患者血浆Apelin水平及脑钠肽（BNP）含量,同时测量左室射血分数（LVEF）、左心室舒张期内径（LVDD）以及左室后壁厚度（LVPW）并进行比较。结果与单纯高血压患者相比,高血压伴心力衰竭患者血浆Apelin水平显著降低（P〈0.05）。年龄增加、BNP水平升高、血浆Apelin水平降低、左室肥厚等与高血压发展为心力衰竭呈正相关（P〈0.05或P〈0.01）。结论在确定高血压伴心力衰竭患者危险分级时血浆Apelin水平可以作为一个观察指标。     

1, 25-Dihydroxyvitamin D3 activates Apelin/APJ system and inhibits the production of adhesion molecules and inflammatory mediators in LPS-activated RAW264.7 cells

Background1, 25-Dihydroxyvitamin D3 (1, 25(OH)₂D₃), an active form of vitamin D3, plays a crucial role in the mitigation of inflammation damage. Recent studies have revealed that apelin and its receptor (apelin/APJ system) could significantly ameliorate LPS-induced inflammation-response. This investigation aimed to appraise the effects of 1, 25(OH)₂D₃ on the apelin/APJ system and production of adhesion molecules and inflammatory mediators in LPS–activated RAW264.7 macrophage cells.MethodsMurine RAW264.7 cells were pretreated with 1, 25(OH)₂D₃, followed stimulation with LPS (1 μg/mL) for 24 h. The effect of 1, 25(OH)₂D₃ on LPS-induced cell injury was determined by MTT assay, whereas, enzyme-linked immunosorbent assay (ELISA), qPCR and western blotting were used to evaluate cytokine production and apelin/APJ system expression. Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) protein expression were measured by flow cytometry.ResultsThe levels of IL-1β, IL-6, and TNF-α cytokines were significantly increased by incubation with LPS. LPS also increased the protein expression of adhesion molecules, including VCAM-1 and ICAM-1. However, pretreatment with 1, 25(OH)₂D₃ markedly inhibited LPS-induced production of inflammatory cytokines and adhesion molecules. Moreover, we found that 1, 25(OH)₂D₃ could induced the apelin/APJ system expression. Further experiments demonstrated the significant increase of apelin/APJ system expression at both the protein and mRNA levels in LPS-activated cells when pretreated with 1, 25(OH)₂D₃.ConclusionTaken together, our results indicated that 1, 25(OH)₂D₃ confers an anti-inflammatory effect through a likely mechanism involving a reduction in pro-inflammatory mediators and adhesion molecules via up-regulation of the apelin/APJ system in RAW264.7 cells.     

老年糖尿病患者血清Apelin水平与尿白蛋白排泄率相关性分析

目的探讨老年糖尿病患者血清Apelin水平与尿白蛋白排泄率的相关性,为老年糖尿病肾病的预治提供临床依据。方法59例年龄在65岁以上的糖尿病患者和30例同年龄段健康对照者,采用酶联免疫吸附法测定空腹血清Apelin含量,同时检测空腹血糖及24小时尿白蛋白排泄率（UAER）,分析其相关性。结果59例糖尿病患者血清Apelin值为473±64．34,UAER为87．34±44．32,两者呈在非常显著的正相关（r=0．384,P〈0．01）。而对照组两指标无相关性。同时糖尿病组和对照组的血清Apelin水平与血糖值之间也无明显相关性。结论老年糖尿病患者血清apelin升高与UAER密切相关,提示血清Apelin水平可能是糖尿病肾病发生的因素之一。     

2型糖尿病患者血浆apelin水平与血管并发症的相关性分析

目的：探讨2型糖尿病患者血浆 apelin 水平与血管并发症的关系及其可能的影响因素。方法选取2型糖尿病患者60例,其中2型糖尿病无血管并发症（ A）组10例,2型糖尿病合并大血管并发症（B）组12例,2型糖尿病合并微血管并发症（C）组10例,2型糖尿病合并微血管及大血管并发症（D）组28例。健康对照组10例。所有受检者测定血浆apelin,同时检测体重指数（ BMI）、腰臀比（ WHR）、血压（BP）、空腹血糖（FPG）、C肽（C-p）、糖化血红蛋白（HbA1c）、尿微量白蛋白（UAER）、血脂及超声心动图等指标,分析2型糖尿病患者血浆apelin的含量与血管并发症的相关性及其可能影响因素。结果2型糖尿病各组（ A、B、C、D）血浆apelin水平显著高于健康对照组,D组血浆apelin水平显著高于A、B、C组,差异有显著性（P〈0.01）;与血浆apelin水平具有统计学意义的相关性因素有FPG（Beta=0.525,P=0.000）、E/A （Beta=-0.210,P=0.005）、HbA1c（Beta=0.237,P=0.019）、SBP（Beta=0.165,P=0.026）;Logistic回归分析结果显示血浆apelin及总胆固醇（ TC）与2型糖尿病大血管并发症存在相关性,血浆apelin与2型糖尿病微血管并发症存在相关性。结论①2型糖尿病患者血浆apelin水平升高,伴随2型糖尿病血管并发症的发生发展,血浆apelin水平有升高趋势,提示血浆apelin与2型糖尿病及其血管并发症相关;②与血浆apelin水平具有显著性的相关性因素有FPG、E/A、HbA1c、SBP;血浆apelin水平随着FPG、HbA1c及SBP的升高而升高;随着左室舒张功能的下降,血浆apelin水平升高,apelin可能成为预测左室舒张功能不全的指标;③血浆apelin水平升高与2型糖尿病大血管并发症和2型糖尿病微血管并发症存在相关性,血浆apelin水平越高,2型糖尿病血管并发症的发生率越高。     

脂肪炎症因子在肾病综合征大鼠肾组织的变化及意义

目的: 观察脂肪炎症因子(Apelin)在阿霉素肾病大鼠模型肾组织中的表达,探讨Apelin与肾病综合征中蛋白尿及高脂血症之间的关系。方法: Wistar大鼠40只,随机分为肾病组32只和正常对照组8只,尾静脉单次注射阿霉素5 mg/kg建立肾病模型,测定24 h尿蛋白排泄量、血清中胆固醇含量,应用免疫组织化学法观察肾皮质中Apelin表达变化,并对Apelin表达与尿蛋白、胆固醇水平进行相关性分析。结果: 肾病组大鼠24 h尿蛋白排泄量、胆固醇含量、肾组织中Apelin蛋白表达量与正常对照组差异均有统计学意义(P < 0.05~P < 0.01),肾病组大鼠肾小球系膜基质增生明显,且Apelin蛋白表达与24h尿蛋白排泄量、血清胆固醇含量呈正相关关系(P < 0.05)。结论: Apelin在肾组织中的表达主要位于肾小球血管袢,随着尿蛋白量、胆固醇水平的增加,肾组织中Apelin蛋白水平亦增加。尿蛋白量及血脂水平与Apelin表达密切相关。     

Circulating levels of Elabela and Apelin in the second and third trimesters of pregnancies with gestational diabetes mellitus

Abstract

We design this study to detect levels of Elabela (ELA) and Apelin (APLN) in women with and without gestational diabetes mellitus (GDM) in the second and third trimesters, and to identify whether there is any association between ELA, APLN, and metabolic parameters. Seventy-nine GDM and 80 control subjects in the second trimester and 87 GDM and 88 healthy subjects in the third trimester were included. In the second trimester, lower ELA levels [(14.1 versus 16.9) ng/ml, p?=?.025] and higher APLN levels [(1021.8 versus 923.5) pg/ml, p?=?.046] were observed in GDM patients compared to controls. ELA levels were positively correlated with fasting plasma glucose (FPG) (r?=?0.423, p?<?.001) in the control group, and APLN levels were negatively correlated with triglycerides (TG) (r?=??0.251, p?=?.025) in the control group and total cholesterol (TC) (r?=??0.227, p?=?.044) in the GDM group. ELA appeared to be related to glucose metabolism and APLN is involved in lipid metabolism during pregnancy. The expression of ELA is significantly downregulated from the second trimester to the third trimester.