血脂康对高脂血症患者小而密低密度脂蛋白的影响

目的:观察血脂康对高脂血症患者血浆小而密低密度脂蛋白(sLDL)的影响。方法:以50例高脂血症患者为治疗组,20例正常健康人为正常对照组。治疗组病人每日口服1.2g血脂康,共服6周。服药前后常规测定血脂。2%～16%非变性梯度凝胶电泳法分离出sLDL,扫描仪半定量分析sLDL的含量,并计算sLDL中的胆固醇(sLDL-C)含量。结果:治疗组服用血脂康后血清TC、低密度脂蛋白-胆固醇(LDL-C)、TG显著降低(P<0.01);治疗组调脂治疗前sLDL占低密度脂蛋白(LDL)的相对值及sLDL-C含量明显高于正常对照组。调脂治疗6周后,治疗组sLDL占LDL的相对值及sLDL-C的实际含量显著下降,分别为44±12vs39±10、1.65±0.31vs1.03±0.21,均为P<0.05。结论:血脂康在调节血脂水平的同时可有效降低sLDL及sLDL-C的含量。     

慢性肾功能衰竭患者小而密低密度脂蛋白的水平变化临床研究

目的探讨慢性肾功能衰竭患者小而密低密度脂蛋白的水平变化临床意义。方法选择我院2011年1月至2012年12月153例江苏省南通大学附属医院分院肾内科住院慢性肾功能衰竭患者为研究对象,进行小而密低密度脂蛋白测定,比较3组不同肾小球滤过率患者小而密低密度脂蛋白差异,进行统计处处理。结果测定结果显示不同肾小球滤过率患者之间小而密低密度脂蛋白水平有显著性差异(P<0.05)。肾小球滤过率<35 m L/min组小而密低密度脂蛋白水平平均为(0.938±0.506)mmol/L高于肾小球滤过率>60 m L/min组的(0.623±0.625)mmol/L(P<0.05),说明随着肾小球滤过率的下降小而密低密度脂蛋白水平也逐步下降。结论慢性肾功能衰竭患者动脉血管硬化机制中,小而密低密度脂蛋白作用可能较小,不能用一般动脉粥样硬化机制进行解释,有待进一步研究。     

血清小而密低密度脂蛋白水平对颈动脉中内膜厚度的影响

目的 探讨血清小而密低密度脂蛋白(sdLDL)水平对颈动脉中内膜厚度(CA-IMT)的影响.方法 行颈部动脉血管超声检查患者217例分为正常组(A组,113例,CA-IMT＜0.9 mm)和增厚组(B组,104例,0.9m≤CA-IMT≤1.5mm).检测并分析血清sdLDL水平与CA-IMT增厚程度的相关性.结果 B组血清sdLDL水平高于A组[(1.0±0.3)mmol/L vs.(0.8±0.4)mmol/L](P＜0.05).sdLDL水平增高者发生CA-IMT增厚的可能性是其正常者发生增厚的3.80倍.sdLDL水平与CA-IMT的增厚程度呈正相关(r=0.757,P＜0.01).结论 血清sdLDL增高是CA-IMT增厚的危险因素,与CA-IMT厚度有较高的相关性.     

小而密低密度脂蛋白胆固醇对颈总动脉内膜中层厚度的诊断价值

目的 探讨血清小而密低密度脂蛋白胆固醇(sdLDL-C)水平对颈总动脉内膜中层厚度(CCA-IMT)的诊断价值。方法根据颈动脉彩色多普勒超声检查结果将250例研究对象分为CCA-IMT增厚(A组,128例)和CCA-IMT正常(B组,122例)两组,采用多因素Logistic回归分析CCA-IMT增厚与其相关危险因素的关系,评价sdLDL-C筛选颈总动脉中内膜增厚的临床效果。结果 sdLDL-C是CCA-IMT增厚的重要影响因素(P<0.05)。sdLDL-C对CCA-IMT诊断的敏感性、特异性和阳性预测值分别为80%、79%和89%。结论sdLDL-C对CCA-IMT增厚有较高的诊断价值。     

小而密低密度脂蛋白胆固醇联合同型半胱氨酸检测对脑梗死老年患者预后评估的价值

目的 分析血清小而密低密度脂蛋白胆固醇（sdLDL-C）联合同型半胱氨酸（Hcy）检测对预测脑梗死老年患者预后评估的价值。方法 选择马鞍山市人民医院2015年2月至2016年2月就诊的46例罹患脑梗死老年患者作为研究对象。检测患者血清sdLDL-C、Hcy、总胆固醇（TC）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、空腹血糖（FBG）、糖化血红蛋白（HbA1c）。随访1年根据是否脑卒中复发及全因死亡进行分组,预后良好组（未发生终点事件）和预后不良组（发生终点事件）。应用logistic回归分析随访1年发生终点事件的危险因素;应用ROC曲线评估血清sdLDL-C及Hcy水平预测脑梗死老年患者随访1年发生终点事件的特异度和敏感度。结果 与预后良好组相比,预后不良组血清sdLDL-C、Hcy、LDL-C及HbA1c较高（P<0.05）,HDL-C较低（P<0.05）,但TC及FBG差异无统计学意义（P>0.05）。多元logistic回归分析,血清sdLDL-C、Hcy水平是脑梗死老年患者随访1年发生终点事件的危险因素（P<0.05）。ROC曲线评估血清sdLDL-C、HCY水平预测脑梗死老年患者随访1年发生终点事件有显著预测价值（P<0.05）,且判定血清sdLDL-C为1.31 mmol/L、血清Hcy为19.9 μmol/L对预测随访1年发生终点事件有88.9%的灵敏和84.6%的特异度。结论 血清sdLDL-C及Hcy检测能有效预测脑梗死老年患者短期发生终点事件的危险性。     

氯沙坦对小而密低密度脂蛋白致培养的人脐静脉内皮细胞损伤的保护作用

目的：观察氯沙坦对小而密低密度脂蛋白(sLDL)致人哜静脉内皮细胞(HUVECs)损伤的保护作用。方法：分离、鉴定 sLDL；用连续监测法测各组细胞乳酸脱氢酶(LDH)漏出量；用丙二醛试剂盒测定各组细胞上清中丙二醛(MDA)浓度；用硝酸还原酶法测定各组细胞分泌的一氧化氮(NO)量；用细胞-酶联免疫吸附法检测细胞膜上细胞间粘附分子-1(ICAM-1)蛋白表达量；反转录-多聚酶链反应(RT-PCR)法检测 ICAM-1mRNA 水平。结果：sLDL 使 HUVECs LDH 漏出增多、MDA 生成增多、NO 分泌减少、ICAM-1 表达增多,氯沙坦对此均有明显抑制作用,且呈剂量依赖性。结论：氯沙坦抑制 sLDL 致体外培养 HUVEcs 的损伤。     

小而密低密度脂蛋白胆固醇与35岁以下青年冠心病患者冠状动脉病变严重程度的关系

目的 探讨小而密低密度脂蛋白胆固醇(sdLDL-C)与35岁以下青年冠心病(冠状动脉粥样硬化性心脏病)患者冠状动脉病变严重程度的相关性.方法 回顾性分析2018年1月至2019年6月因胸痛于首都医科大学附属北京安贞医院行冠状动脉造影检查,并被确诊为冠心病的18～35岁青年患者293例的临床资料.冠心病严重程度用改良Ge...     

小而密低密度脂蛋白、Mac-2结合蛋白在急性缺血性脑卒中中的变化及作用研究

目的 探讨小而密低密度脂蛋白(sdLDL)、Mac-2 结合蛋白(M2BP)在急性缺血性脑卒中(AIS)中的变化及作用。方法 选择 2020 年 9 月～2021 年 10 月牡丹江医学院附属红旗医院神经内科确诊的 100 例 AIS 患者(AIS 组)和100 例健康体检人员(对照组)为研究对象,AIS 组根据颈动脉狭窄程度分为轻度组、中度组、重度组,根据 NIHSS 评分将脑卒中患者分为轻度组、中度组、重度组,比较不同组别血清 sdLDL、M2BP 水平,分析血清 sdLDL、M2BP 水平与 AIS患者颈动脉狭窄程度及脑卒中严重程度的关系。结果 AIS 组血清 sdLDL、M2BP 水平高于对照组(P<0.05);随着颈动脉狭窄程度及脑卒中严重程度的加重,血清中 sdLDL、M2BP 水平升高(P<0.05)。Pearson 相关性分析结果显示,M2BP与同型半胱氨酸(Hcy)、sdLDL、NIHSS 评分均呈正相关(r=0.898、0.864 和 0.824,P<0.05),sdLDL 与 Hcy、M2BP、NIHSS评分均呈正相关(r=0.820、0.864...     

阿司匹林抑制ox-LDL诱导内皮细胞炎症分子表达的研究

目的评价阿司匹林对ox-LDL刺激内皮细胞炎症蛋白表达的影响。方法使用培养人脐带内皮细胞,用氧化型低密度脂蛋白刺激内皮细胞16h,终止反应后用SDS-PAGE分离蛋白,使用Western Blot分析蛋白表达的变化。ROS测定使用DCFH-DA荧光标记,用流式细胞仪测定荧光强度。结果①阿司匹林抑制ox-LDL诱导内皮细胞COX-2表达。使用ox-LDL刺激内皮细胞16h,COX-2表达增加,分别用2.5mmol·L-1和5mmol·L-1阿司匹林处理内皮细胞30min后,COX-2表达明显降低。②阿司匹林降低ox-LDL诱导的内皮细胞ICAM-1表达。ox-LDL刺激内皮细胞16h后,Western Blot结果显示ICAM-1内皮细胞表达明显增加。用免疫荧光染色的方法观察细胞获得了同样的结果,ox-LDL刺激后ICAM-1在内皮细胞膜上表达明显增加,阿司匹林处理后减少了ICAM-1在膜上的表达。③阿司匹林轻度抑制ox-LDL诱导内皮细胞ROS产生。0.3g·L-1ox-LDL刺激内皮细胞16h后细胞内ROS明显增高,但阿司匹林仅部分阻止ROS的产生。结论非甾体类抗炎药物阿司匹林对ox-LDL诱导COX-2、ICAM-1有明显的抑制作用,但不能完全阻止ox-LDL诱导的ROS产生。这些结果表明阿司匹林能够减轻氧化脂质诱导的内皮细胞炎症损伤反应。     

Oxidized low-density lipoprotein inhibits vascular endothelial growth factor-induced endothelial progenitor cell differentiation

1. Bone marrow-derived endothelial progenitor cells (EPC) in the peripheral blood of adult animals and humans have been shown to be incorporated into neovascularization. In contrast, hypercholesterolaemia impairs angiogenesis and collateral vessel formation in response to regional tissue ischaemia. We investigated whether oxidized LDL (oxLDL) affected human EPC differentiation. 2. When isolated human mononuclear cells (MNC) were incubated with vascular endothelial growth factor (VEGF), the number of differentiated, adherent EPC, as assessed by an in vitro culture assay, was increased in a dose-dependent manner (P < 0.01). When MNC were incubated with oxLDL at 1, 5 and 10 microg/mL in the presence of 100 ng/mL VEGF for 24 h, oxLDL dose-dependently reduced the number of differentiated, adherent EPC. 3. Vascular endothelial growth factor-induced EPC differentiation was significantly inhibited by pharmacological phosphatidylinositol 3-kinase blockers (either 10 nmol/L wortmannin or 10 micromol/L LY294002). Interestingly, immunoblotting analysis revealed that oxLDL dose-dependently led to dephosphorylation and, thus, deactivation of Akt in the presence of VEGF. Finally, these inhibitory effects induced by oxLDL were abolished by pretreatment with 1 micromol/L atorvastatin (P < 0.01). 4. Our data indicate that oxLDL inhibits VEGF-induced EPC differentiation through the dephosphorylation of Akt.     

氧化低密度脂蛋白对细胞滋养细胞浸润能力的影响

目的:探讨不同浓度氧化低密度脂蛋白(oxLDL)对细胞滋养细胞浸润能力的影响.方法:采用蛋白印迹法和RT-PCR技术检测不同浓度oxLDL(0.01,0.02,0.05,0.1 mg/mL)刺激下细胞滋养细胞中过氧化物酶体增殖物激活受体γ(PPARγ)蛋白及其mR-NA的表达:并检测相应浓度oxLDL对细胞滋养细胞能力的影响.结果:(1)不同浓度oxLDL(0.01,0.02,0.05,0.1mg/mL)刺激下细胞滋养细胞中PPAR-γ蛋白表达水平(15.0±2.0,18.4±2.8,21.3±2.4,25.8±3.0)与对照组(13.3±2.2)比较差异有统计学意义(P<0.01),各组分别比较差异亦有统计学意义P<0.01;(2)不同浓度oxLDL(0.01,0.02,0.05,0.1 mg/mL)刺激下细胞滋养细胞PPARγmRNA表达水平(14.9±3.1,17.2±4.0,19.4±3.2,21.7±3.0)与对照组(12.1±3.3)比较差异有统计学意义P<0.01,各组分别比较差异亦有统计学意义P<0.01;(3)不同浓度oxLDL(0.01,0.02,0.05,0.1mg/mL)刺激下细胞滋养细胞浸润指数(0.66±0.04,0.58±0.03,0.46±0.04,0.32±0.05),与对照组(0.69±0.05)比较差异有统计学意义P<0.01,各组分别比较差异亦有统计学意义P<0.01;(4)oxLDL浓度与细胞滋养细胞的浸润指数呈负相关,(r=-0.98,P<0.01);与细胞滋养细胞PPARγmRNA表达水平呈正相关(r=0.93,P<0.01).结论:oxLDL浓度升高可上调细胞滋养细胞中PPARγ的表达,从而影响细胞滋养细胞的浸润能力.     

Strategies to achieve low-density lipoprotein cholesterol targets in high-risk patients

Several options exist in very-high risk patients who do not achieve low-density lipoprotein cholesterol (LDL-C) targets despite treatment with atorvastatin 80?mg, including switching to rosuvastatin 40 mg, adding ezetimibe or adding a proprotein convertase subtilisin/kexin type 9 inhibitor. Taking into account the safety, LDL-C lowering capacity, effect on cardiovascular events and cost of these available options, switching to rosuvastatin 40?mg appears to represent the most attractive strategy. Nevertheless, more studies are needed to confirm the effects of this strategy on LDL-C levels given the limited available data.     

Reduction of oxidative stress and modulation of autoantibodies against modified low-density lipoprotein after rosuvastatin therapy

AIMS: To examine the effect of 24 weeks' rosuvastatin treatment on oxidative stress and changes in immune response to oxidized low-density lipoprotein (LDL). METHODS: This was an open-label study of patients in Austria receiving 10 or 40 mg rosuvastatin daily alternately during 12 and 24 weeks. Circulating concentrations of antibodies to malondialdehyde-oxidized LDL (MDA-LDL), both IgG and IgM type, to copper-oxidized LDL (Cu-OxLDL-IgG), concentrations of oxidized LDL complexed to IgG (OxLDL-IC) and markers of oxidative stress and systemic inflammation in subjects with plasma LDL cholesterol concentrations between 130 mg dl-1 and 250 mg dl-1 and triglycerides相似文献   

Oxidized low-density lipoprotein induces endothelial progenitor cell senescence, leading to cellular dysfunction

1. Recent studies have revealed an association between coronary risk factors and both the number and function of bone marrow-derived endothelial progenitor cells (EPC). We investigated the effect of oxidized low-density lipoprotein (ox-LDL) on the senescence of EPC, leading to cellular dysfunction. 2. Endothelial progenitor cells were isolated from human peripheral blood and characterized. The exposure of cultured EPC to ox-LDL (10 microg/mL) significantly accelerated the rate of senescence compared with control during 20 days in culture as determined by acidic beta-galactosidase staining. Oxidized LDL-induced EPC senescence was significantly inhibited by pretreatment with either lectin-like ox-LDL receptor-1 (LOX-1) antibody (Ab) or atorvastatin (P < 0.01). 3. Because cellular senescence is critically influenced by telomerase, which elongates telomeres, we measured telomerase activity using a polymerase chain reaction-ELISA-based assay. Oxidized LDL significantly diminished telomerase activity to approximately 50%, an effect that was significantly abolished by pretreatment with either LOX-1 Ab or atorvastatin (P < 0.01). 4. We examined whether ox-LDL-induced EPC senescence translates into EPC dysfunction. An MTS assay disclosed an inhibitory effect of ox-LDL on EPC proliferation. In a Matrigel assay, EPC treated with ox-LDL were less likely to participate in network formation compared with controls. 5. In conclusions, ox-LDL accelerates the onset of EPC senescence, which may be related to telomerase inactivation. Oxidized LDL-induced EPC senescence leads to the impairment of proliferative capacity and network formation.     

Failure of N-acetylcysteine to reduce low-density lipoprotein oxidizability in healthy subjects

Summary We have studied the effects of N-acetylcysteine which is thought to have antioxidant properties, on the susceptibility of low-density lipoprotein to oxidation and on whole-blood glutathione concentrations in six healthy volunteers.N-acetylcysteine was given orally in a dosage of at 1.2 g per day for 4 weeks, followed by 2.4 g per day for a further two weeks. The susceptibility of low-density lipoprotein toin vitro Cu²⁺-oxidation was determined by continuously measuring the formation of conjugated dienes. Whole-blood concentrations of reduced and oxidized glutathione were also determined.N-acetylcysteine had no effect on the susceptibility of LDL to oxidation. Concentrations of vitamin E in the serum and in low-density lipoprotein were not changed. Compared with controls the concentration of glutathione in N-acetylcysteine treated subjects was reduced (–48 %) and the concentration of oxidized glutathione was higher (+80%). The GSH/GSSG-ratio, a marker of oxidative stress was 83 % lower.The results do not support the supposed antioxidative action of N-acetylcysteine. It seems more likely that N-acetylcysteine acts as a pro-oxidant in the dosage used.     

非诺贝特降低生活方式干预无效的脂肪肝患者LDL的疗效

目的调查单用生活方式干预治疗与同时口服非诺贝特治疗非酒精性脂肪肝患者脂代谢紊乱的疗效。方法纳入经6个月的生活方式干预治疗后仍具有脂代谢紊乱的非酒精性脂肪肝患者,口服非诺贝特每日100mg,同时继续进行生活方式干预治疗。结果在52例参加了6个月的生活方式干预治疗的非酒精性脂肪肝患者中,21例仍有脂代谢紊乱的患者被纳入临床研究。纳入患者年龄58(27~75)岁,体质量63.0(39.4~109.0)kg,体质量指数25.4(18.2~37.1)kg·m-2,ALT 23(14~73)IU·L-1,TG 105(92~216)mg·dL-1,HDL 58(37~93)mg·dL-1,LDL 153(66~209)mg·dL-1。21例患者在使用非诺贝特治疗6月后,20例患者中15例(15/20,75%,P=0.001 5)血LDL水平得到改善,5例患者血LDL水平未见明显下降。1例患者口服非诺贝特后出现皮肤瘙痒及皮疹,退出了研究。结论对伴脂代谢紊乱的非酒精性脂肪肝患者,经生活方式干预治疗后脂代谢紊乱未见改善,在联合使用降血脂药物非诺贝特后,脂代谢紊乱可得到改善。     

Serum low-density lipoprotein and high-density lipoprotein cholesterol,and liver size in subjects on drugs inducing hepatic microsomal enzymes

Summary Serum low-density lipoprotein cholesterol and high-density lipoprotein cholesterol concentration and the ratio between them, major risk factors of coronary heart disease, and liver size were investigated in 18 subjects who were on enzyme-inducing anti-convulsants, phenytoin alone or in combination with phenobarbital and/or carbamazepine. The subjects with a high liver cytochrome P-450, indicating hepatic microsomal enzyme induction, who showed an increase in liver size, had an elevated high-density lipoprotein concentration and high-density lipoprotein cholesterol/total cholesterol ratio, and a reduced low/high-density lipoprotein cholesterol ratio. The high-density lipoprotein cholesterol concentration and its ratio to total cholesterol were directly and related to the ratio between low and high-density lipoprotein cholesterol were inversely related to the extent of liver enlargement. The serum cholesterol distribution profile associated with an increase in liver size was typical of subjects with a low risk of coronary heart disease. The results suggest that enzyme-inducers, such as phenytoin and phenobarbital, induce structural and functional changes in hepatocellular membranes associated with liver enlargement and cholesterol distribution characteristic of low susceptibility to atherosclerotic vascular disease.