氧化型低密度脂蛋白与2型糖尿病

糖尿病是一种严重影响人民健康的全球性公共卫生问题，其患病率逐年升高，在中国糖尿病患病人数住居世界第二。2型糖尿病已成为世界上第三大危害人类健康的疾患。氧化型低密度脂蛋白（oxidized low density lipoprotein，ox-LDL）是LDL氧化修饰的产物，研究表明其在2型糖尿病的各种并发症中起着很重要的作用，近年来受到许多国内外学者的关注。该文对氧化型低密度脂蛋白与2型糖尿病之间的关系作一综述，为2型糖尿病患者的病情观察和疗效判断作出科学依据。     

氧化型低密度脂蛋白促动脉硬化机制

动脉粥样硬化（As）是一种复杂的炎症性疾病,主要症状为动脉壁增厚变硬,失去弹性及管腔狭小等。其伴随的病理特征主要为动脉某些部位内膜下脂质沉积,伴有平滑肌细胞和纤维基质成分的增殖,并逐步发展形成动脉硬化斑块。研究发现低密度脂蛋白（LDL）,尤其是氧化型低密度脂蛋白（ox-LDL）在 As 的发病形成过程中起着重要作用。     

葛根素对氧化型低密度脂蛋白的影响

研究证明葛根索治疗不稳定型心绞痛(UA)的疗效确切。我们在治疗冠心病的同时发现ox-LDL的水平下降，观察总结如下。     

氧化型低密度脂蛋白、糖基化低密度脂蛋白与糖尿病肾病的关系

近年来的研究表明[1],LDL经氧化修饰后形成的氧化修饰低密度脂蛋白(oxidized low-density lipoprotein,OXLDL)可以通过多种途径影响糖尿病合并动脉粥样硬化的发生。LDL在高血糖的状态下,经非酶糖化形成糖基化低密度脂蛋白(glycosylated low-density lipoprotein,GLDL),由于糖化过程中氧自由基的产生,使GLDL或LDL更易氧化为OXLDL,而GLDL、OXLDL均可使血管病变发生率增加。本研究通过糖尿病肾病(DN)患者血液OXLDL、GLDL等含量的测定,探讨OXLDL与GLDL的关系及其在DN中的作用。1研究对象和方法1.12型糖尿病及DN患者为我…     

动脉硬化患者氧化型低密度脂蛋白的定量研究

目的　为探讨氧化型低密度脂蛋白 (Ox -LDL)对动脉粥样硬化的致病作用和临床意义。方法　我们利用克隆抗体酶联免疫吸附试验 ,定量测定了 2 0 0例急性心脑血管病患者和 2 0 0例健康对照者血浆中氧化型低密度脂蛋白 (Ox -LDL)的水平。结果　显示急性心脑血管病患者血中Ox -LDL含量 (886 .7± 2 48.9μg/L) ,明显高于对照组 (32 3.1± 83.0 μg/L)。 结论　血中氧化型低密度脂蛋白参与与动脉粥样硬化的发病 ,抗低密度脂蛋白的氧化修饰是预防和治疗心脑血管疾病的重要措施。     

氧化低密度脂蛋白与动脉粥样硬化

氧化低密度脂蛋白与动脉粥样硬化庄一义作者单位：２１０００２南京军区南京总医院全军医学检验中心血清低密度脂蛋白（ＬＤＬ）增高是动脉粥样硬化（ＡＳ）的重要危险因素，但在早期ＡＳ病变中，泡沫细胞的主要前驱——单核巨噬细胞在体外不能迅速、大量摄取天然ＬＤＬ形...     

脑卒中与氧化低密度脂蛋白

目的 :了解氧化低密度脂蛋白 (OXLDL)与脑卒中发病的关系。方法 :用ELISA法检测 10 3例脑卒中患者血清OXLDL ,与 60例健康体检者比较。结果 :脑卒中组血清OXLDL的 x±s为 :69.93± 3 9.64mg/L ;健康体检者为3 9.2 3± 19.0 6;经统计学检验 ,脑卒中组血清OXLDL显著升高 (P <0 .0 0 1)。结论 :OXLDL可作为脑卒中致病的重要危险因素之一 ;测定血清OXLDL值是预测脑卒中发病的重要参数之一。     

氧化型低密度脂蛋白与冠状动脉病变程度的关系

目的 探讨血浆氧化修饰低密度脂蛋白(OX-LDL)与冠状动脉病变程度的关系。方法 采用酶免疫吸附法测定OX-LDL，同时用酶法测定血脂、免疫透射比浊法测定载脂蛋白水平。结果 冠心病组OX-LDL、低密度脂蛋白胆固醇(LDL-C)、TGC、TG、ApoB、及LP（a)较对照组增高，而HDL-C、ApoA1降低，且冠状动脉病变程度越重，OX-LDL越高。结论 血浆OX-LDL水平与冠状动脉粥样硬化及其程度显著相关．测定其水平对评价冠心病的程度有一定临床意义。     

冠心病氧化型低密度脂蛋白自身抗体影响因素分析

目的 探讨冠心病患者血清氧化型低密度脂蛋白自身抗体(ox-LDLab)的影响因素.方法 选择冠心病患者为研究对象,分为稳定型心绞痛组(SAP组)、不稳定型心绞痛组(UAP组)和急性心肌梗死(AMI组),另以正常健康人为对照组(CON组),比较四组研究对象BMI指数、脉压(PP)、常规生化指标和ox-LDLab的差异,分析ox-LDLab与相关因素的关糸.结果 四组研究对象BMI指数、PP、FBG和HbA1c差异无统计学意义(P>0.05);SAP组、UAP组和AMI组患者TC、TG、LDL、LP(a)和ox-LDLab显著高于CON组(P<0.05),HDL显著低于CON组(P<0.05);SAP组、UAP组和AMI组患者TC、TG、LDL、HDL、LP(a)和ox-LDLab差异有统计学意义(P<0.05).SAP组、UAP组和AMI组患者ox-LDLab与BMI指数、PP、FBG和HbA1C无相关性(P>0.05),与TC、TG、LDL和LP(a)正相关(rs>0,P<0.05),与HDL负相关(rs<0,P<0.05).结论 冠心病患者血清ox-LDLab显著高于正常人,血脂是其主要的影响因素.     

氧化型低密度脂蛋白与冠状动脉病变程度的关系

目的探讨血浆氧化修饰低密度脂蛋白(OX-LDL)与冠状动脉病变程度的关系.方法采用酶免疫吸附法测定OX-LDL,同时用酶法测定血脂、免疫透射比浊法测定载脂蛋白水平.结果冠心病组OX-LDL、低密度脂蛋白胆固醇(LDL-C)、TC、TG、ApoB、及LP(a)较对照组增高,而HDL-C、ApoA1降低,且冠状动脉病变程度越重,OX-LDL越高.结论血浆OX-LDL水平与冠状动脉粥样硬化及其程度显著相关,测定其水平对评价冠心病的程度有一定临床意义.     

Oxidized low density lipoproteins, statin therapy and severity of coronary artery disease

BACKGROUND: The impact of statin therapy on the association between circulating levels of oxidized low density lipoproteins (OxLDL) and severity of coronary artery disease (CAD) has not been studied. METHODS: OxLDLs were measured in 687 patients with angiographically proven CAD (320 patients, 46.6% on statin therapy and 367 patients, 53.4% not on statin therapy on admission) using the Mercodia Oxidized LDL Enzyme-Linked Immunosorbent Assay (ELISA). RESULTS: Patients on statin therapy had lower levels of OxLDL (median [interquartile range]; 63.9 U/L [53.9; 79.8] versus 72.3 U/L [58.4; 86.1], P<0.001) and C-reactive protein (3.0 mg/L [1.2; 6.6] versus 4.0 mg/L [1.7; 13.1], P<0.001) than patients not on statins. Multivariable analysis showed that statin therapy was an independent predictor of lower levels of OxLDL (P=0.0001). In univariate analysis, OxLDL level did not differ significantly among the patients with 1-, 2-or 3-vessel disease (70.5 U/L [57.5; 85.6], 66.3 U/L [53.8; 82.6] and 68.2 U/L [57.0; 83.4], respectively, P=0.26). Multivariable logistic regression analysis showed that OxLDL was an independent correlate of angiographic severity of CAD (P=0.04) and that there was an interaction (P=0.038) between statins and OxLDL in that the increased levels of OxLDL were associated with more extensive CAD. CONCLUSION: Patients with CAD who receive statins have lower levels of OxLDL and an attenuation of the relationship between circulating levels of OxLDL and CAD severity compared with patients who do not receive statins.     

Oxidized low density lipoproteins cause contraction and inhibit endothelium-dependent relaxation in the pig coronary artery.

The direct vasoactive effects of native and oxidatively modified low density lipoproteins as well as their effects on endothelium-dependent relaxations to 5-hydroxytryptamine were studied in isolated rings of pig right coronary artery. Slowly developing contractions were caused by native low density lipoproteins (100 micrograms protein/ml). The contractions were more pronounced in the absence than in the presence of the trace metal chelator, EDTA, and coincided with the formation of lipid peroxides during the response. The lipophilic antioxidant, butylated hydroxytoluene, prevented the oxidation of, and contraction to, native low density lipoproteins. Low density lipoproteins oxidized by exposure to copper contracted coronary arteries more rapidly with a threshold of only 1 micrograms protein/ml, but with a similar maximal contraction at 100 micrograms protein/ml. Superoxide dismutase inhibited the contraction to native low density lipoproteins, but not to oxidized low density lipoproteins. Catalase blocked contractions to both native and oxidized low density lipoproteins. Contractions to oxidized low density lipoproteins were unaffected by indomethacin, but were abolished by removal of the endothelium or by inhibitors of endothelium-derived relaxing factor. Oxidized low density lipoproteins but not native low density lipoproteins inhibited endothelium-dependent relaxations to 5-hydroxytryptamine. Thus, oxidized low density lipoproteins caused endothelium-dependent coronary artery contractions which are mediated by a hydroperoxide. Contractions to native low density lipoproteins are due to their oxidation in the organ chamber by the superoxide anion radical. Oxidized, but not native, low density lipoproteins impair normal endothelial cell vasodilator function in vitro. Oxidized low density lipoproteins, important in the pathogenesis of atherosclerosis, may directly contribute to the increased risk of vasospasm seen in hypercholesterolemia and atherosclerosis.     

氧化低密度脂蛋白刺激内皮细胞程序性死亡配体-1的表达

目的:研究氧化低密度脂蛋白(ox-LDL)对人脐静脉内皮细胞的负性共刺激分子程序性死亡因子配体-1(PD-L1)袁达的影响,探讨动脉粥样硬化发病的免疫机制.方法:体外培养人脐静脉内皮细胞,并分别与不同浓度(10、50、100 mg/L)ox-LDL温育24 h,以PBS作阴性对照,采用逆转录聚合酶链反应、流式细胞技术分别检测人脐静脉内皮细胞PD-L1的mRNA及蛋白表达水平.结果:随着ox-LDL浓度的增加,人脐静脉内皮细胞的PD-L1表达逐步升高,低浓度(10 mg/L)OX-LDL与对照组比较差异无统计学意义,中浓度(50 mg/L)及高浓度(100 mg/L)ox-LDL组较对照组PD-L1表达显著升高,差异有统计学意义(P＜0.05).结论:公认有致慢性炎症作用的ox-LDL刺激人脐静脉内皮细胞炎症反应时,上调负性共刺激分子PD-L1的表达,这种负反馈调节可能是抑制动脉粥样硬化的一种免疫机制.     

Oxidized low-density lipoprotein and atherosclerosis

Atherosclerosis is the leading cause of morbidity and mortality in western society. The most important risk factors for atherosclerosis include smoking, hypertension, dyslipidemia, diabetes and a family history of premature atherosclerosis. Several studies indicate that an increased plasma low density lipoprotein (LDL) cholesterol constitutes a major risk factor for atherosclerosis. Many data support a proatherogenic role for oxidized LDL and its in vivo existence. The oxidative susceptibility of LDL is increased with established cardiovascular risk factors, such as diabetes, smoking and dyslipidemia. Supplementation with antioxidants such as ascorbate and alpha-tocopherol can decrease LDL oxidation as well as cardiovascular mortality and thus shows promise in the prevention of atherosclerosis.     

Oxidized lipoproteins and endothelium.

Endothelium is an early target of pro-atherosclerotic events, which may result in functional and morphological perturbations. Oxidized low density lipoproteins, an atherogenic factor with strong cytotoxicity, may potentially contribute to altered endothelial function through the activation of a stress response, which would rescue cells to full vitality, or, conversely, by leading to cell death. Evidence is presented here for the ability of chemically oxidized low density lipoproteins to induce the synthesis of the inducible form of heat shock protein 70 in cultured human endothelial cells, and for the association of epitopes of these modified lipoproteins with apoptotic endothelial cells in aortic sections from hypercholesterolemic rabbits.