瑞舒伐他汀联合缬沙坦对急性冠状动脉综合征患者高敏C反应蛋白及脑钠肽的影响

目的探讨瑞舒伐他汀联合缬沙坦对急性冠状动脉综合征(ACS)患者高敏C反应蛋白(hs-CRP)及N端前脑钠肽(NT-proBNP)的影响。方法将90例ACS住院患者随机分为A、B、C三组各30例,A组口服瑞舒伐他汀10mg,B组口服瑞舒伐他汀10mg+缬沙坦80mg,C组口服阿托伐他汀20mg+缬沙坦80mg,均1次/d,服药4周,治疗前和治疗4周后抽取静脉血,观察三组治疗前后血清hs-CRP及NT-proBNP水平。结果治疗4周后,三组血清hs-CRP及NT-proBNP水平均较治疗前明显降低(P<0.01),其中B组及C组较A组降低更明显(P<0.01)。结论 ACS患者早期联合使用瑞舒伐他汀及缬沙坦可明显减轻炎性反应、改善心功能。     

瑞舒伐他汀对急性冠脉综合征患者PCI术后疗效和血清因子表达的影响

目的 分析对急性冠脉综合征患者行PCI(经皮冠状动脉介入治疗)术后应用瑞舒伐他汀的具体效果和实际应用价值。方法 选取本院2017年1月～2019年1月急性冠脉综合征患者PCI术后患者124例,依据随机数字表法将其分为四组,每组31例,A组术前服用安慰剂,术后服用小剂量瑞舒伐他汀;B组术前服用40mg瑞舒伐他汀,术后服用小剂量瑞舒伐他汀;C组术前服用40mg瑞舒伐他汀,术后服用大剂量瑞舒伐他汀;D组术前服用80mg瑞舒伐他汀,术后服用大剂量瑞舒伐他汀。比较四组患者服药前后血脂水平、白介素18(IL-18)和高敏C反应蛋白(hs-CRP)和总有效率。结果 服药前,四组患者血清总胆固醇(TC)和甘油三酯(TG)水平差异无统计学意义(P 0.05);服药后,C组血脂水平明显低于其他三组,差异具有统计学意义(P 0.05)。治疗前,四组患者IL-18和hs-CRP水平差异无统计学意义(P 0.05);治疗后,C组患者IL-18和hs-CRP水平明显低于其他三组,差异具有统计学意义(P 0.05)。A组、B组、C组和D组总有效率分别为70.97%、70.97%、90.32%和74.19%,C组明显高于其他三组,差异具有统计学意义(P 0.05)。结论 在急性冠脉综合征患者行PCI术前服用40mg瑞舒伐他汀,且术后按照20mg/d的剂量口服,可以显著改善体内炎性因子水平,调节血脂,整体效果较好,在临床上具有重要应用价值。     

不同剂量瑞舒伐他汀早期干预对急性冠脉综合症患者血脂及hs-CRP的影响

目的探讨不同剂量瑞舒伐他汀早期干预治疗对急性冠脉综合症(ACS)患者血脂及血清高敏C反应蛋白的影响。方法 100例ACS患者随机分为大剂量瑞舒伐他汀(1日40mg)治疗组(50例)和常规剂量瑞舒伐他汀(1日20mg)治疗组(50例),分别在入院24h内及服药后3d、7d测定患者血脂、高敏C反应蛋白,比较两组患者血脂、高敏C反应蛋白的变化。结果治疗7d后1日20mg及1日40mg瑞舒伐他汀治疗组总胆固醇、低密度脂蛋白水平较治疗前有降低(P<0.05),而且1日40mg瑞舒伐他汀治疗组高敏C反应蛋白水平显著降低,与1日20mg瑞舒伐他汀治疗组比较有显著差异(P<0.01),而治疗前后两组总胆固醇、低密度脂蛋白比较无统计学意义(P>0.05)。结论早期大剂量瑞舒伐他汀应用更能降低ACS患者的高敏C反应蛋白水平,且瑞舒伐他汀的抗炎治疗独立于降脂之外。     

瑞舒伐他汀对急性冠脉综合征患者PCI术后疗效和血清因子表达的影响

目的观察瑞舒伐他汀用于急性冠脉综合征（ACS）经皮冠状动脉介入治疗（PCI）术前及术后对围操作期心肌梗死、血脂水平（TG、TC、LDL-C）、血清炎性因子[高敏C反应蛋白（hs-CRP）、白介素18（IL-18）]及脂联素（APN）水平的影响,为找到更适合用于急性冠脉综合征治疗的他汀类药物提供依据。方法采用前瞻性、双盲、随机对照研究方法,180例行PCI术的急性冠脉综合征患者,随机分为实验1组（术前口服安慰剂,术后瑞舒伐他汀10mg/d口服24周）、实验2组（术前口服瑞舒伐他汀40mg、术后10mg/d口服24周）、实验3组（术前口服瑞舒伐他汀40mg、术后20mg/d口服24周）、实验4组（术前口服阿托伐他汀80mg,术后20mg/d口服24周）,每组均为45例。观察PCI围操作期心肌梗死的发生情况在各组间的差别;观察术前及术后多个时点的血脂水平及APN、hs-CRP、IL-18的表达在各组间的差别。结果实验2组、3组、4组的围操作期心肌梗死少于实验1组（P〈0.05）。在术后4、12、24周,1～3组降低TC、LDL-C的效果好于4组,其中3组效果最佳。hs-CRP及IL-18水平在术后48h时2、3、4组均低于1组,其中3组最低;在术后4、12、24周时1、2、3组均低于4组,仍为3组最低。脂联素在术后4~24周逐渐升高,升高幅度由高到低的排序为：3组、2组和1组、4组。结论 PCI术前服瑞舒伐他汀能减少急性冠脉综合征行PCI术患者的围操作期心肌梗死;瑞舒伐他汀具有比等效剂量的阿托伐他汀更好的降脂、降低急性冠脉综合征患者血清hs-CRP、IL18及升高APN的作用,从而具有更好的抗炎、抗动脉粥样硬化的作用;临床应用20mg/d瑞舒伐他汀比10mg/d具有更好的效果。     

瑞舒伐他汀对急性冠脉综合征患者支架植入术后炎症因子和近期预后的影响

目的探讨瑞舒伐他汀对非ST段抬高的急性冠脉综合征(ACS)经皮冠脉支架植入(PCI)患者术后血清炎症因子及近期预后的影响。方法 90例非ST段抬高的ACS患者随机均分为瑞舒伐他汀负荷剂量组(A组,20mg/d)、瑞舒伐他汀常规剂量组(B组,10mg/d)和阿托伐他汀组(C组,20mg/d),测定术前和术后24h血清内皮素1(ET-1)、基质金属蛋白酶9(MMP-9)、超敏C反应蛋白(hsCRP)的变化,随访6个月心脏不良事件的发生率。结果与术前比较,A、B、C组术后ET-1、MMP-9和hsCRP水平均增加,A组ET-1、MMP-9和hsCRP水平增幅小于B、C组(P<0.05)。A组术后6个月心脏不良事件发生率低于B组和C组(6.90%vs.13.3%和14.3%)(P<0.05和P<0.01)。结论早期应用负荷量瑞舒伐他汀可减少非ST段抬高的ACS患者PCI术后炎症因子的增加,降低术后6个月心脏不良事件发生率。     

阿托伐他汀对中年女性急性冠脉综合征介入术后的影响

目的:探讨阿托伐他汀治疗中年女性急性冠脉综合征(ACS)经皮冠状动脉介入治疗(PCI)术后炎性因子的变化,同时监测其调脂疗效及不良事件发生率.方法:入选60例女性ACS患者经PCI后,均给予阿托伐他汀40mg治疗,其中中年女性(40～59岁)组30例,老年女性(60～75岁)组30例,分别在术前、术后即刻、术后1周、术后1个月,分别抽血查高敏C反应蛋白(hs-CRP)、TG、TC、LDL-C、HDL-C及ALT、AST、CK.结果:(1)中年女性组血脂异常患病率低于老年女性组;(2)中年女性组与老年女性组术前hs-CRP比较差异无统计学意义(P＞0.05);(3)两组术后即刻hs-CRP均高于术前(P＜0.05);(4)两组在术后1周及1个月hs-CRP均有明显降低(P＜0.05).结论:中年女性ACS患者虽然血脂异常率低,但其炎性因子水平仍有明显增高,使用阿托伐他汀能明显降低血清炎性因子水平,减少冠状动脉粥样斑块炎性反应.     

不同剂量瑞舒伐他汀对AMI患者血浆SAA、Hs-CRP、N-pro-BNP水平的影响

目的观察不同剂量瑞舒伐他汀对急性心肌梗死（acute myocardial infarction,AMI）患者血浆血清淀粉样蛋白A（SAA）、超敏C反应蛋白（hs-CRP）、N末端B型脑钠肽前体（NT-pro-BNP）水平的影响。方法 56例急性心肌梗死患者经PCI后,接受常规治疗,随机分为两组：A组（n=28）给予瑞舒伐他汀（10mg/d）,B组（n=28）强化剂量（20mg/d）治疗,两组疗程均为3个月,观察心血管事件发生情况。并设健康对照组（n=24）。结果与对照组相比,A、B两组血清hs-CRP、SAA、NT-pro-BNP水平显著升高（P〈0.05）;治疗后1、2周A、B两组血清hsCRP、SAA、NT-pro-BNP水平均明显下降,差异有统计学意义（P〈0.05）;且B组下降幅度更大,差异有统计学意义（P〈0.05）。随访3个月B组总心血管事件发生率明显低于A组,差异有统计学意义（P〈0.05）。结论 PCI术后给予强化瑞舒伐他汀治疗短期即可显著降低血清炎性因子,且疗效优于常规治疗剂量,有利于AMI患者的恢复。     

不同剂量瑞舒伐他汀对急性冠脉综合征患者血清sOX40L、MMP-9的影响

目的　探讨不同剂量瑞舒伐他汀对急性冠脉综合征（ACS）患者血清可溶性OX40配体（sOX40L）、基质金属蛋白酶9（MMP-9）的影响。方法　选择ACS患者60例,空白对照组20例。随机将ACS患者分为20 mg瑞舒伐他汀治疗组（20mg组）30例和10 mg瑞舒伐他汀治疗组（10mg组）30例,比较治疗前后各组间血清sOX40L、MMP-9的水平变化。结果　瑞舒伐他汀治疗2周后,两治疗组患者血清sOX40L、MMP-9水平均较治疗前明显降低,差异有统计学意义（P<0.01）。其中20mg组较10mg组降低更为明显,差异有统计学意义（P<0.05）。 结论　ACS患者早期使用较大剂量瑞舒伐他汀可明显减少冠状动脉粥样斑块基质成分的降解和炎症反应,从而起到稳定动脉粥样硬化斑块,改善ACS患者的预后的作用。     

不同剂量瑞舒伐他汀对急性冠状动脉综合征患者血浆hs-CRP水平的影响

目的观察急性冠状动脉综合征(ACS)患者早期给予不同剂量瑞舒伐他汀短期治疗对血浆hs-CRP的影响。方法 83例ACS患者随机分为A、B两组,在常规治疗的基础上分别给予瑞舒伐他汀20mg/d和40mg/d顿服,疗程7d,分别测定治疗前后血浆hs-CRP水平。结果治疗后两组hs-CRP水平均下降,与治疗前比较差异有显著性(P<0.05);B组较A组下降明显,差异有显著性(P<0.05)。结论急性冠状动脉综合征患者早期给予强化瑞舒伐他汀治疗可明显降低血浆hs-CRP的水平。     

氟伐他汀联合普罗布考对急性冠脉综合征患者血脂及血清hs-CRP水平的影响

目的:探讨氟伐他汀联合普罗布考对急性冠脉综合征(ACS)患者血脂及血清超敏C-反应蛋白(hs-CRP)水平的影响。方法:收集ACS住院患者60例,随机分为A、B、C3组,每组20例,A组给予氟伐他汀40mg,1次/晚;B组给予氟伐他汀80mg,1次/晚;C组给予氟伐他汀40mg,1次/晚,并加用普罗布考250mg,2次/d。3组患者均于治疗前清晨空腹取血,测定hs-CRP和血脂水平,包括总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)。结果:治疗前3组间各项血脂指标及hs-CRP水平差异均无统计学意义(P0.05)。治疗后C组血脂指标和hs-CRP水平较A组均降低(P0.05),TC及HDL-C水平较B组均低(P0.05),而TG及LDL-C水平与B组比较差异无统计学意义(P0.05)。治疗后B、C组中TC、TG、LDL-C水平较治疗前降低(P0.05或P0.01);各组hs-CRP水平治疗前后差异均有统计意义(P0.05)。结论:氟伐他汀联合普罗布考或大剂量氟伐他汀均能明显降低ACS患者血脂及hs-CPR水平,尤以氟伐他汀联合普罗布考效果更为显著。     

血液透析冠心病患者低密度脂蛋白/高密度脂蛋白与氧化应激的临床研究

目的:探讨血液透析冠心病患者血脂低密度脂蛋白(LDL)/高密度脂蛋白(HDL)与氧化应激的临床意义。方法:采用回顾性方法分析2010年1月—2013年12月住院的所有血液透析合并冠心病患者临床资料。对照组为无冠心病者33例,观察组为冠心病者20例,分别检测各组患者LDL,HDL、血清晚期蛋白氧化产物(AOPPs)、血清超氧化物歧化酶(SOD)及丙二醛(MDA)等变化。结果:两组的HDL及LDL/HDL比较,差异有统计学意义(P<0.05),两组的SOD,MDA及AOPPs比较,差异有统计学意义(P<0.05)。提示冠心病患者中LDL明显升高,而HDL明显降低,同时存在明显的氧化应激产物水平升高。采用逐步回归相关分析研究,经过逐步拟合,得出回归方程:y=6.884-4.811X2+1.249X3-0.057X4,结果表明LDL/HDL比值与LDL,HDL及SOD存在线性回归关系。由标准回归系数看出LDL/HDL比值与LDL关系最大。结论:在血液透析冠心病患者中,其血脂LDL/HDL比值变化可能与氧化应激之间存在一定的相关性。     

High‐density lipoproteins,platelets and the pathogenesis of atherosclerosis

1. Prospective and interventional studies demonstrate an inverse relationship between plasma high‐density lipoprotein (HDL)–cholesterol and the incidence of coronary artery disease. Although the atheroprotective effects of HDL are usually attributed to the reverse cholesterol transport, in which HDL shuttles cholesterol from cells in the arterial wall to the liver, other mechanisms are also under investigation. 2. Platelets are involved in both the initiation and progression of atherosclerotic lesions. In addition, the formation of thrombi over ruptured atherosclerotic plaques results in the narrowing or complete occlusion of coronary arteries. Current experimental evidence suggests that HDL may exert antiplatelet effects and thereby counteract the development of atherothrombotic vascular disease. 3. In vitro studies show that HDL inhibits agonist‐stimulated platelet aggregation, fibrinogen binding, granule secretion and liberation of thromboxane A₂. Inhibitory effects of HDL are mediated, in part, by scavenger receptor type B1 and/or the apolipoprotein E receptor apoER2/LRP8 and are linked to the induction of intracellular signalling cascades encompassing stimulation of protein kinase C, cytoplasmatic alkalization and generation of nitric oxide. 4. Populational studies demonstrate that there is an inverse association between plasma HDL levels and recurrent venous thromboembolism. In addition, HDL–cholesterol has been identified as an independent predictor of acute platelet thrombus formation. The administration of reconstituted HDL particles in humans attenuates ex vivo platelet activation. 5. The present review summarizes recent advances in understanding HDL–platelet interactions and discusses the potential use of HDL‐like particles in the therapy of thrombosis.     

Synthetic nano-low density lipoprotein as targeted drug delivery vehicle for glioblastoma multiforme

The low density lipoprotein (LDL) receptor has been shown to be upregulated in GBM tumor cells and is therefore a potential molecular target for the delivery of therapeutic agents. A synthetic nano-LDL (nLDL) particle was developed and tested to determine its utility as a drug delivery vehicle targeted to GBM tumors. nLDL particles were constructed by combining a synthetic peptide containing a lipid binding motif and the LDL receptor (LDLR) binding domain of apolipoprotein B-100 with a lipid emulsion consisting of phosphatidyl choline, triolein, and cholesteryl oleate. Composition analysis, fast protein liquid chromatography, and electron microscopy revealed that nLDL was highly reproducible and intermediate in size between high density lipoprotein and LDL particles (10.5+/-2.8 nm diameter). The binding and uptake of fluorescently labeled nLDL particles was assessed using fluorescence microscopy. Uptake of nLDL was time dependent, exhibiting saturation at approximately 3 h, and concentration dependent, exhibiting saturation at concentrations greater than 5 microM peptide. Using Lysotracker as a cellular marker, nLDL co-localized with lysosomes. nLDL binding was eliminated by blocking LDLRs with suramin and nLDL inhibited binding of plasma LDL to LDLRs. Collectively these data strongly suggest that the synthetic nano-LDLs described here are taken up by LDLR and can serve as a drug delivery vehicle for targeting GBM tumors via the LDLR.     

Impact of short‐term low‐dose atorvastatin on low‐density lipoprotein and high‐density lipoprotein subfraction phenotype

Statins can significantly reduce low‐density lipoprotein–cholesterol (LDL‐C) and modestly raise or not alter high‐density lipoprotein–cholesterol (HDL‐C). However, their impact on high‐density lipoprotein (HDL) and low‐density lipoprotein (LDL) subfractions has been less examined. The aim of the present study was to investigate the short‐term impact of low‐dose atorvastatin on HDL and LDL subfractions in humans. In this randomized study, data from 52 subjects were analysed. Thirty‐seven patients with atherosclerosis were randomized to treatment with atorvastatin 10 mg/day (n = 17) or 20 mg/day (n = 20) for 8 weeks, with 15 healthy subjects without therapy used as a control group. The lipid profile and lipoprotein subfractions were determined using the Lipoprint system at baseline and at 8 weeks. The data suggest that atorvastatin treatment (10 and 20 mg/day) for 8 weeks significantly decreases LDL‐C levels and reduces the cholesterol concentration of all LDL subfractions, which is accompanied by an increase of the mean LDL particle size. Although 10 mg/day atorvastatin treatment for 8 weeks had no impact on the HDL subfraction, 20 mg/day atorvastatin for 8 weeks significantly increased the cholesterol concentration of large HDL particles and decreased the cholesterol concentration of small HDL particles without changing serum HDL‐C levels in patients with atherosclerosis. Therefore, the results suggest that 20 mg/day atorvastatin treatment for 8 weeks may result in a favourable modification of the HDL subfraction phenotype in addition to its effects on the cholesterol concentration of all LDL subfractions and mean LDL particle size.     

虎杖苷通过降血脂抗ApoE-/-小鼠动脉粥样硬化的作用

目的 研究虎杖苷在ApoE-/-小鼠动脉粥样硬化治疗中的作用及其可能的机制。方法 采用高脂饲料连续喂养12周ApoE-/-小鼠,建立动脉粥样硬化动物模型,将已经形成动脉粥样硬化ApoE-/-小鼠分为模型对照组,虎杖苷组,阳性药（辛伐他汀）对照组,每组8只,阳性药（辛伐他汀）以0.05 (g·kg-1·d-1)灌胃,虎杖苷含生药0.2 (g·kg-1·d-1)灌胃,空白正常对照组及模型对照组分别给予同体积的蒸馏水,连续ig 28 天后,取血和冠状动脉,采用H&E染色对冠状动脉的形态学改变进行观察;检测血清中高密度脂蛋白,氧化型的低密度脂蛋白,总胆固醇的含量。结果 病理切片H&E染色显示给药虎杖苷后,小鼠的血管组织形态较模型组有较明显的改善,和阳性药组结果类似,显示出虎杖苷对动脉粥样硬化具有较好的的治疗效果;与模型组比较,虎杖苷可以显著（p P < 0.05）的降低血清中氧化型低密度脂蛋白的水平。 结论 虎杖苷可降低血脂,减少脂质的沉积,改善动脉粥样硬化血管组织的形态,具备治疗动脉粥样硬化的潜力。     

氧化低密度脂蛋白和同型半胱氨酸与循环内皮细胞和内皮素在冠心病患者血浆中的相关性

目的:探讨循环内皮细胞、内皮素、氧化低密度脂蛋白和同型半胱氨酸与动脉粥样硬化发生过程中的关系,以及氧化低密度脂蛋白和同型半胱氨酸与循环内皮细胞和内皮素之间的相关性。方法:分别用酶联免疫吸附法和高效液相色谱分析法测定血浆中氧化低密度脂蛋白和同型半胱氨酸水平,同时测定血浆中循环内皮细胞和内皮素水平,进行对比和直线相关性分析。结果:冠心病组循环内皮细胞7.78±3.31cells/0.9μL,内皮素98.14±35.08 ng/L,氧化低密度脂蛋白809.25±311.89μg/L,同型半胱氨酸19.40±7.03μmol/L。对照组上述指标分别为:4.10±1.60cells/0.9μl,52.61±15.71ng/L,438.24±200.54μg/L和11.19±2.94μmol/L。两组比较差异有显著性P<0.001。冠心病组血氧化低密度脂蛋白与血浆循环内皮细胞、内皮素均呈正相关,相关系数分别为0.926(P<0.001)、0.979(P<0.001),同型半胱氨酸同样与循环内皮细胞、内皮素呈正相关,相关系数分别为0.947(P<0.001)、0.900(P<0.001),且冠心病组血浆循环内皮细胞和内皮素呈正相关,相关系数为0.939(P<0.001)。结论:氧化低密度脂蛋白和高同型半胱氨酸可能造成VEC损伤及功能改变,对动脉粥样硬化的发生发展有促进作用。     

Effects of ethyl-CPIB (clofibrate) on tissue lipoprotein lipase and plasma post-heparin lipolytic activity in rats

The role of LPL in reducing the serum triacylglycerol concentration was investigated in rats fed a high sucrose diet containing 0.25% (w/w) ethyl-CPIB. Compared with sucrose-fed controls, drug treatment resulted in a fall in adipose tissue LPL activity and a rise in enzyme activity in thigh and heart muscle. Serum post-heparin lipoprotein lipase activity after a high dose of heparin was lower in ethyl-CPIB-treated rats than controls, but after a low dose of heparin the values were similar. The amount of LPL activator was decreased by the drug. Thus, the low serum triacylglycerol concentration observed in the ethyl-CPIB-treated rats cannot be explained by changes in functional LPL activity. The plasma triacylglycerol-lowering effect of the drug could be explained by the observed decrease in triacylglyerol output by the liver.     

高密度脂蛋白与载脂蛋白A1、低密度脂蛋白与载脂蛋白B的相关性分析

目的对高密度脂蛋白与载脂蛋白A1、低密度脂蛋白与载脂蛋白B之间的相关性进行分析探讨。方法随机抽取在2010年1月～2012年5月间在本院进行体检的500名受检者,对其进行血清高密度脂蛋白(HDL-C)、低密度脂蛋白(LDL-C)、载脂蛋白A1(apoA1)、载脂蛋白B(apoB)测定,并按照三酰甘油(TG)水平的不同进行分组,分析HDL-C与apoA1、LDL-C与apoB之间的相关性。结果在TG水平小于10.00mmol/L时,HDL-C与apoA1、LDL-C与apoB之间存在明显的相关性,在TG水平大于10.00mmol/L时,HDL-C与apoA1、LDL-C与apoB不具有明显的相关性。结论在一定条件下,HDL-C与apoA1、LDL-C与apoB存在比较明显的相关性,这将对临床诊断与治疗评价产生重要意义,值得关注。     

Activation of membrane outward currents by human low density lipoprotein in mouse peritoneal macrophages

Summary The aim of the present study was to search for electrophysiological effects of human lipoproteins on membrane currents in mouse peritoneal macrophages which had been cultured for 5 to 20 days. Whole-cell currents were recorded by using a voltage-clamp technique.Low density lipoprotein (LDL, 100 g/ml) increased a slowly activating nonspecific cation current (i_so) in the positive potential range to 244 ± 23% of the reference (test potential + 55 mV, n = 13, P < 0.005). Augmentation of current resulted out of a negative shift of the activation curve along the voltage axis (–22 mV) and an increase of maximally available current.Furthermore, LDL increased a rapidly activating outward current (i_fo) at test potentials positive to the potassium equilibrium potential. At +55 mV i_fo-amplitude increasedto 165 ± 14% ofreference (n = 16, P < 0.005). LDL-induced effects on i_fo-current could be mimicked by application of the calcium ionophore A 23187 (1 mol/l) which led to an increase of i_fo-current to 161 ± 25% of the reference (test potential + 55 mV, n = 11, P < 0.005).Acetylated-LDL (100 g/ml, 5–15 min) produced no significant effect on the membrane currents under investigation. Correspondence to U. Borchard at the above address     

人血高密度脂蛋白生物活性测定方法的研究

目的 :建立人血高密度脂蛋白 (HDL)生物活性检测法。方法 :根据受体酶联免疫检测法的原理和步骤 ,以超速离心制备的HDL为参考品 ,以每 1 μgapoAⅠ为一个HDL活性单位 ,通过HDL生物活性标准曲线双对数回归方程 ,求测待测HDL制剂的生物活性。结果 :标准曲线在 1～ 1 6个活性单位范围内呈线性关系。测定的板内及板间变异系数分别为 7.6 %～ 9.5 %及 1 2 .3%。结论 :此法操作简便 ,重复性好 ,且HDL以外的脂蛋白不干扰检测反应 ,可作为检测人血浆HDL制剂生物活性的方法。