姜黄素对脂多糖联合干扰素γ诱导的巨噬细胞炎症因子表达的影响及其机制

目的探讨姜黄素对脂多糖联合干扰素γ诱导的巨噬细胞表达炎症因子的影响及其相关机制。方法用脂多糖联合干扰素γ诱导巨噬细胞构建炎症细胞模型并设立不同浓度的姜黄素干预组和对照组,通过实时荧光定量PCR及酶联免疫吸附法测定不同分组中肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)及白细胞介素12B(IL-12B)三种炎症因子的表达。Western blot检测各组细胞TLR4-MAPK/NF-κB信号通路的表达。结果实时荧光定量PCR显示,与对照组相比,姜黄素对脂多糖联合干扰素γ诱导的巨噬细胞TNF-α、IL-6及IL-12B m RNA的表达均具有明显抑制作用(P0.001),酶联免疫吸附法也证实姜黄素能抑制以上炎症因子的分泌(P0.01)。Western blot检测显示,姜黄素能明显抑制TLR4的表达及下游MAPK(p38、ERK1/2及JNK1/2)和NF-κB(IκBα及p65)通路的磷酸化(P0.05)。结论姜黄素可通过抑制TLR4-MAPK/NF-κB信号通路抑制脂多糖联合干扰素γ诱导的巨噬细胞中TNF-α、IL-6及IL-12B这三种炎症因子的表达。     

TLR4介导汉滩病毒引起血管内皮细胞分泌IL-6和TNF-α

目的检测汉滩病毒感染血管内皮细胞后IL-6,IL-8和TNF-α的分泌变化及其与TLR4的关系。方法用5LgTCID50/mL的HTNV76-1180.2mL感染EVC-304细胞(TLR4+)和EVC-304TS4(TLR4-)分别为实验组,以病毒未感染为阴性对照组,以LPS(2μg/mL)刺激作为阳性对照。48h后取细胞培养上清,用人IL-6,IL-8和TNF-α定量EIA试剂盒分别检测IL-6,IL-8和TNF-α在两个细胞系感染前后的分泌水平。结果IL-8在两个细胞系中感染前后的变化不明显,IL-6和TNF-α在EVC-304细胞系中,HTNV感染后升高,而在TLR4表达阴性的EVC-304细胞中,感染前后变化不明显。结论在TLR4表达阳性的EVC-304细胞中IL-6和TNF-α分泌增加,血管内皮细胞EVC-304在HTNV感染后的IL-6和TNF-α分泌可能是TLR4介导的。     

锌指蛋白A20抑制Toll样受体4介导的人单核细胞炎症反应的实验研究

目的:观察锌指蛋白A20过度表达对人单核细胞膜Toll样受体(TLR4),下游促炎因子肿瘤坏死因子-α(TNF-α)与白细胞介素(IL)-12,以及抗炎因子IL-10表达的影响,探讨锌指蛋白A20对单核细胞炎症反应的抑制作用及可能的调节机制。方法:Ficoll细胞分离液分离人外周血单核细胞,随机分为对照组、脂多糖(LPS)组、A20转染组与LPS+A20转染组。荧光显微镜检测GFP报告基因,免疫组织化学检测A20蛋白的表达,RT-PCR检测A20及TLR4的mRNA表达,流式细胞检测技术检测TLR4的蛋白表达,ELISA方法检测上清液TNF-α、IL-12及IL-10表达水平。结果:LPS刺激后,单核细胞TLR4和内源性A20的mRNA和蛋白、TNF-α、IL-12和IL-10表达较对照组均明显升高(均P<0.01);TNF-α/IL-10和IL-12/IL-10均明显高于对照组(均P<0.01);转染A20基因的单核细胞,在无LPS刺激的条件下,上述指标与对照组相比均差异无统计学意义;转染A20基因的单核细胞在LPS刺激后,TLR4mRNA和蛋白、TNF-α、IL-12的表达以及TNF-α/IL-10和IL-12/IL-10均显著低于LPS组,而IL-10的表达明显高于对照组和LPS组(均P<0.01)。结论:TLR4激活介导单核细胞的炎症反应,且正反馈调节其自身受体TLR4和内源性A20的表达;A20参与单核细胞TLR4激活所介导的炎症反应,其表达增加与TLR4表达的增加有关;单纯提高A20表达对未被激活的单核细胞TLR4及其信号通路影响不大;A20过表达可抑制TLR4激活所介导的单核细胞的炎症反应。     

乌司他丁对内毒素血症大鼠心肌TOLL样受体4表达的影响

目的 观察乌司他丁对脂多糖(Lipopolysaccharides,LPS)诱导心肌TOLL样受体4(TLR4)受体表达的影响及与炎症反应的关系.方法 选取8周龄的雄性SD大鼠32只,分成四组:正常对照组,内毒素血症组(LPS组),LPS+乌司他丁组,LPS+地塞米松组.除正常对照组以外,其余三组给予脂多糖8 mg/kg大鼠阴茎静脉注射,LPS+乌司他丁组与LPS+地塞米松组分别同时给予乌司他丁2.5万/kg、地塞米松5 mg/kg;正常对照组给予同量的生理盐水,3h后断头取血并取心肌液氮保存;ELISA法测血浆TNF-α的水平;放免法测定心肌组织中AngⅡ水平;RT-PCR法测定心肌组织TLR4 mRNA表达;免疫组化法和蛋白免疫印迹法测心肌组织TLR4含量.结果 (1)LPS组TNF-α、CRP、IL-6水平和心肌AngⅡ水平显著增高;与LPS组相比,乌司他丁组TNF-α 、CRP、IL-6和心肌AngⅡ显著降低(2)LPS可明显增加心肌中TLR 4 mRNA及蛋白表达,乌司他丁明显抑制心肌TLR4 mRNA及蛋白的表达.结论 乌司他丁能抑制LPS诱导大鼠心肌的炎症反应.乌司他丁能降低LPS诱导大鼠的心肌TLR4 mRNA及蛋白的表达.乌司他丁可能通过降低TLR4水平抑制LPS诱导的炎症反应.     

过表达Krüppel样因子9对脂多糖诱导的肺泡上皮细胞损伤的影响及机制

目的:探讨Krüppel样因子9(KLF9)对脂多糖(LPS)诱导的人肺泡上皮细胞A549增殖、凋亡和炎症的影响及机制。方法:A549细胞随机分为四组:NC组、LPS组、LPS+pcDNA-con组和LPS+pcDNA-KLF9组。qRT-PCR检测KLF9、IL-6、IL-1β和TNF-αmRNA的表达,MTT法检测细胞活力,流式细胞术检测细胞凋亡情况,Western blot检测KLF9、CyclinD1、Bax、Bcl-2、β-catenin和GSK-3β蛋白的表达。结果:与NC组相比,LPS组的细胞存活率显著降低,细胞凋亡率显著增加,KLF9、CyclinD1和Bcl-2蛋白的表达显著降低,Bax蛋白和炎症因子IL-6、IL-1β和TNF-α的表达显著升高;与LPS+pcDNA-con组相比,LPS+pcDNA-KLF9组细胞存活率显著升高,细胞凋亡率显著降低,KLF9、CyclinD1和Bcl-2蛋白的表达显著升高,Bax蛋白和炎症因子IL-6、IL-1β和TNF-α的表达显著降低(P<0.05)。过表达KLF9可抑制LPS诱导的A549细胞中Wnt/β-catenin信号通路的激活。结论:过表达KLF9可减轻脂多糖诱导的肺泡上皮细胞损伤,这可能与抑制Wnt/β-catenin信号通路有关。     

芍药苷对脂多糖诱导的THP-1细胞炎症因子分泌和ABCA1表达的影响

目的观察芍药苷(PF)对脂多糖(LPS)诱导的THP-1细胞炎症因子和三磷酸腺苷结合盒转运体A1(ABCA1)表达的影响。方法用含PF(10-8、10-7、10-6、10-5、10-4mol/L)培养基预处理细胞0.5 h,再用含LPS(1mg/L)培养基共同培养细胞24 h。ELISA检测细胞培养液上清中白细胞介素1β(IL-1β)、白细胞介素6(IL-6)、白细胞介素8(IL-8)和肿瘤坏死因子α(TNF-α)水平,Western blot检测细胞中ABCA1蛋白的表达。结果与对照组比较,LPS组细胞上清液中IL-1β、IL-6、IL-8和TNF-α的水平显著性升高(P0.05),ABCA1蛋白表达显著性下调(P0.05)。与LPS组比较,LPS+PF(10~(-6)、10~(-5)和10~(-4)mol/L)组上清液中IL-1β、IL-6、IL-8和TNF-α的水平显著性降低(均P0.05),ABCA1蛋白表达显著性上调(P0.05),呈现浓度依赖性。结论芍药苷抑制LPS诱导的THP-1细胞炎症因子分泌和ABCA1表达下调。     

人参皂苷Rb1通过抑制PI3K/AKT信号通路保护脂多糖诱导的心肌细胞炎症反应

目的探究人参皂苷Rb1在脂多糖(LPS)诱导的H9C2心肌细胞炎症反应中的作用及分子机制。方法建立LPS诱导的H9C2心肌细胞炎症反应模型。在用1μg/ml的LPS诱导H9C2心肌细胞炎症反应前,使用100μM人参皂苷Rb1或1μM PI3K抑制剂Wortmannin预处理1 h,2 h后收集细胞样本。利用q PCR检测白介素-6(IL-6),白介素-1β(IL-1β),肿瘤坏死因子-α(TNF-α)的m RNA表达水平;用ELISA试剂盒检测细胞上清IL-6,IL-1β,TNF-α的蛋白表达;用WB实验检测p-AKT和AKT的表达水平。结果人参皂苷Rb1显著抑制LPS诱导的IL-6,IL-1β,TNF-α的m RNA(P0.001)和蛋白(P0.001)表达水平;人参皂苷Rb1显著抑制LPS诱导的PI3K/AKT信号通路的激活(P0.001);PI3K抑制剂Wortmannin也能显著抑制LPS诱导的p-AKT表达水平以及IL-6,IL-1β,TNF-α的m RNA(P0.001)和蛋白(P0.001)表达水平。结论人参皂苷Rb1通过抑制PI3K/AKT信号通路阻止LPS诱导的心肌细胞炎症反应。     

细胞因子和脂多糖对人结肠癌细胞系HT-29 Toll样受体4表达和调控的影响

背景：正常肠上皮作为物理屏障能限制肠道微生物的入侵。肠上皮细胞极低表达Toll样受体（TLR）4和髓样分化蛋白（MD）-2，不与脂多糖（LPS）反应。目的：探讨以细胞因子肿瘤坏死因子（TNF）-α、白细胞介素（IL）-1β、干扰素（IFN）-γ和LPS刺激人结肠癌细胞系HT-29后，TLR4和MD-2的表达及其对LPS反应性的变化。方法：将FIT-29细胞分为8组，分别加入RPMI1640、TNF-α、IL-1β、IFN-γ、LPS、TNF-α＋LPS、IL-1β＋LPS、IFN-γ＋LPS干预；酶联免疫吸附测定（ELISA）检测各组细胞上清液内IL-8水平；逆转录聚合酶链反应（RT-PCR）检测各组细胞TLR4和MD-2 mRNA的表达。结果：TNF-α、IL-1β和IFN-γ能显著上调HT-29细胞TLR4、MD-2 mRNA和IL-8的表达（P〈0．01）；HT-29细胞与，TNF-α、IL-β、IFN-γ预孵育后再以LPS刺激，IL-8的表达进一步上调（P〈0．01）。结论：细胞因子（TNF-α，IL-1β，IFN-γ）可增加肠上皮细胞TLR4和MD-2的表达，促进其对LPS的反应，引起肠上皮细胞对常驻菌的过度反应．从而启动或加重肠道炎症。     

酰基化Ghrelin在体外拮抗巨噬细胞介导的炎症反应对胰岛β细胞功能影响的研究

目的 采用Transwell小室构建的小鼠胰岛细胞株MIN6和巨噬细胞株RAW264.7共培养系统,探讨酰基化Ghrelin能否保护胰岛β细胞免遭巨噬细胞介导的炎症损伤. 方法 实验分为单独RAW264.7巨噬细胞组、单独MIN6胰岛细胞组、共培养组和Ghrelin干预组.RT-PCR和Western blot 检测巨噬细胞上Toll样受体4(TLR4)和脂肪酸结合蛋白(A-FABP)的表达;ELISA检测细胞上清液IL-1β、TNF-α的浓度,以及葡萄糖刺激后MIN6细胞上清液的胰岛素浓度. 结果 (1)共培养系统中,巨噬细胞TLR4[mRNA及蛋白水平分别为(1.35±0.13),(0.93±0.03)],A-FABP[(1.99±0.10)vs(0.91±o.01)]的表达],细胞上清液IL-1β[(10.47±1.11) pg/ml]、TNF-α[(917.54±9.09) pg/ml]蛋白水平较单独RAW264.7巨噬细胞组高(P＜0.05);(2)高糖刺激下,共培养系统中胰岛β细胞的胰岛素分泌水平较单独MIN6胰岛细胞组低(P＜0.05);(3)与共培养组比较,酰基化Ghrelin干预后共培养,巨噬细胞TLR4表达水平和TNF-α均降低(P＜0.05),且呈剂量依赖性,但胰岛β细胞的胰岛素分泌水平与共培养组比较,差异无统计学意义(P＞0.05). 结论 巨噬细胞与胰岛β细胞共培养后,炎症通路活化,炎症因子释放,胰岛β细胞的胰岛素分泌功能受损;酰基化Ghrelin可剂量依赖性削弱巨噬细胞和胰岛β细胞共培养后炎症通路的活化和炎症因子的释放,但不能完全阻止胰岛β细胞胰岛素分泌功能的降低.     

乙型肝炎病毒转染及脂多糖刺激对HepG2细胞Toll样受体2和4表达的影响

目的探讨乙型肝炎病毒(HBV)转染对HepG2细胞表面Toll样受体(TLR)表达的影响及脂多糖(LPS)加重HBV转染致肝细胞损伤是否存在直接作用,进一步探讨乙型肝炎发病及重型化的发生机制。方法以不同浓度的LPS刺激HepG2细胞、HepG2．2．15细胞(转染HBV全基因组的HepG2细胞),并以免疫细胞化学方法检测HepG2细胞及HepG2．2．15细胞表面TLR 2、4蛋白质表达情况,以逆转录聚合酶链反应(RT-PCR)检测TLR2、4 mRNA表达情况,用Abbot试剂检测HepG2．2．15细胞HgsAg和HgeAg表达情况,用流式细胞仪观察细胞生长周期及细胞凋亡情况。结果HepG2、HepG2．2．15细胞膜上均有TLR2、4蛋白质表达,免疫细胞化学染色在未加LPS及各浓度LPS刺激细胞均可见细胞膜有棕褐色着色,且随着LPS浓度增加,其着色强度增加;对0mg/L及10mg/L LPS诱导HepG2、HepG2．2．15细胞RNA进行RT-PCR扩增,其产物行10g/L琼脂糖凝胶电泳均可见特异性条带,且10mg/L LPS诱导细胞TLR2和TLR4与分子量标准品的吸光度值比值明显高于0mg/L LPS诱导细胞扩增产物,分别为306．63±6．18对519．84±9．15和700．54±13．56对1116．62±37．67,F值分别为740．58和426．07,P值分别为0．01和0．02;流式细胞仪检测细胞周期发现HepG2绌胞及未经LPS诱导的HepG2．2．15未发生凋亡,各浓度LPS诱导的HepG2．2．15细胞均有细胞凋亡发生,且细胞凋亡率随着LPS浓度增加上升。结论LPS可能通过其与肝细胞膜上的TLR结合,而参与HBV转染后肝细胞损害及肝脏炎症重型化的发病机制。     

Plasma apolipoprotein E concentration is an important determinant of phospholipid transfer protein activity in type 2 diabetes mellitus

BACKGROUND: Phospholipid transfer protein (PLTP) transfers phospholipids between lipoproteins and plays an important role in HDL metabolism. PLTP exists as a high-activity and a low-activity form in the circulation. In vitro studies have shown that apolipoprotein (apo) E is involved in maintaining PLTP in the active form, while the low-activity form is associated with apo AI. We have therefore investigated whether plasma apo AI, B and E concentrations are important determinants of plasma PLTP activity in type 2 diabetes, a condition associated with increased plasma PLTP activity. METHODS: Plasma PLTP activity was assayed by measuring the transfer of radiolabelled phosphatidylcholine from liposomes to HDL; apo AI and B by rate nephelometry and apo E by a 2-point turbidimetric assay. RESULTS: Type 2 diabetic patients (n = 230) had higher PLTP activity than controls (n = 97) (2374 +/- 628 nmol/mL/h versus 1862 +/- 585 respectively, p < 0.01). They also had increased fasting triglyceride and low HDL. Plasma apo B (p < 0.01) and apo E (p < 0.05) were increased, whereas apo AI was reduced (p < 0.01). Univariate analysis showed that plasma PLTP activity correlated mainly with apolipoproteins AI and E. Stepwise regression analysis showed that apo E was the main determinant of plasma PLTP activity, accounting for 23% of its variability in the diabetic subjects and 8% in the controls respectively. CONCLUSIONS: The associations between plasma apo AI and E concentrations and PLTP activity suggest that these apolipoproteins are important regulators of PLTP activity in vivo. The increase in PLTP activity in type 2 diabetes is partly related to the changes in these apolipoproteins.     

Influence of apolipoprotein E genotype on the response to caloric restriction in type 2 diabetic patients with hyperlipidaemia

Aims:  Hyperlipidaemia is a major predisposing factor to atherosclerosis in patients with type 2 diabetes. Apolipoprotein (apo) E polymorphism influences lipoprotein metabolism, and the present study was undertaken to explore the relation, in type 2 diabetics, between apo E genotype and the plasma lipid response to dietary therapy.
Methods:  The subjects were 104 patients with type 2 diabetes and hyperlipidaemia, and the difference, due to apo E genotype, in dietary response was followed for 4–6 weeks. The caloric intake was maintained in the range 20–25 kcal/kg, and the medications for diabetes were not changed during the follow-up period.
Results:  Plasma total cholesterol (TC) and triglyceride (TG) levels were significantly lowered by the dietary treatment in patients with apo E genotypes of ε3/3, ε2/3 and ε3/4; however, the lipid levels in patients with ε2/4 did not respond to the diet.
Conclusions:  apo E genotype should be taken into consideration in the treatment of hyperlipidaemia in diabetic patients.     

脂蛋白肾病患者载脂蛋白E基因全长序列分析

目的：通过对脂蛋白肾病患者载脂蛋白E(apoE)基因的全长序列分析，探讨apoE基因突变与脂蛋白肾病发病之间的关系。方法：对5例正常对照和17例脂蛋白肾病患者的apoE基因全长经PCR扩增后进行测序分析。结果：①与正常对照相比，17例脂蛋白肾病患者未发现存在apoE基因突变；②未发现国外已报道的脂蛋白肾病相关apoE基因突变类型；③中国汉族人apoE基因与GenBank中相应基因序列有10处非编码区的序列差异，这种差异在正常人和脂蛋白肾病患者之间无差异。结论：①在本研究范围内，未发现脂蛋白肾病患者存在apoE基因突变；②apoE基因非编码区在不同种族间存在差异。     

Health-protective and adverse effects of the apolipoprotein E epsilon2 allele in older men

OBJECTIVES: To reexamine a health‐protective role of the common apolipoprotein E (APOE) polymorphism focusing on connections between the APOE?2—containing genotypes and impairments in instrumental activities of daily living (IADLs) in older (≥65) men and women and to examine how diagnosed coronary heart disease (CHD), Alzheimer's disease, colorectal cancer, macular degeneration, and atherosclerosis may mediate these connections. DESIGN: Retrospective cross‐sectional study. SETTING: The unique disability‐focused data from a genetic subsample of the 1999 National Long Term Care Survey linked with Medicare service use files. PARTICIPANTS: One thousand seven hundred thirty‐three genotyped individuals interviewed regarding IADL disabilities. MEASUREMENTS: Indicators of IADL impairments, five geriatric disorders, and ?2‐containing genotypes. RESULTS: The ?2/3 genotype is a major contributor to adverse associations between the ?2 allele and IADL disability in men (odds ratio (OR)=3.09, 95% confidence interval (CI)=1.53–6.26), although it provides significant protective effects for CHD (OR=0.55, 95% CI=0.33–0.92), whereas CHD is adversely associated with IADL disability (OR=2.18, 95% CI=1.28–3.72). Adjustment for five diseases does not significantly alter the adverse association between ?2‐containing genotypes and disability. Protective effects of the ?2/3 genotype for CHD (OR=0.52, 95% CI=0.27–0.99) and deleterious effects for IADLs (OR=3.50, 95% CI=1.71–7.14) for men hold in multivariate models with both these factors included. No significant associations between the ?2‐containing genotypes and IADL are found in women. CONCLUSION: The ?2 allele can play a dual role in men, protecting them against some health disorders, while promoting others. Strong adverse relationships with disability suggest that ?2‐containing genotypes can be unfavorable factors for the health and well‐being of aging men.     

Apolipoprotein E genotype affects the response to lipid-lowering therapy in Chinese patients with type 2 diabetes mellitus

OBJECTIVE: To evaluate the effect of apolipoprotein E (apoE) genotype on baseline lipid levels and the response to hydroxy-methyl glutaryl coenzyme A reductase inhibitors (statins) therapy in Chinese patients with type 2 diabetes mellitus (DM). RESEARCH DESIGN AND METHODS: We consecutively recruited Chinese patients with type 2 DM requiring lipid-lowering therapy according to current guidelines. Patients were started on either simvastatin 10 mg daily or given an equivalent dose of lovastatin 20 mg. After 12 weeks of statin therapy, patients had fasting lipid profiles repeated. ApoE genotyping was performed by restriction fragment length polymorphism (RFLP). RESULTS: Ninety-six patients were studied. The epsilon3/epsilon3 genotype was in 62.5%, epsilon2/epsilon3 and epsilon3/epsilon4, 16.7 and 20.8%, respectively. After adjusting for confounding variables, baseline total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels were significantly higher in those with epsilon3/epsilon4 compared with epsilon2/epsilon3 genotype (6.7 vs. 5.5 mm for TC, 4.5 vs. 3.6 mm for LDL-C; p = 0.015 and p = 0.025, respectively). With statin therapy, epsilon3/epsilon4 patients had significantly greater LDL-C lowering compared with epsilon2/epsilon3 patients (48 vs. 27.7%; p = 0.04). There was no gender difference in baseline lipid parameters or response to statin therapy. CONCLUSIONS: ApoE genotype accounts for interindividual variability of baseline cholesterol levels, and response to statin therapy in Chinese patients with type 2 DM.     

Expression of type III hyperlipoproteinaemia in a subject with secondary hypothyroidism bearing the apolipoprotein E2/2 phenotype

Post-surgical hypothyroidism developed in a now 43-year-old woman with complete insufficiency of the anterior pituitary gland who discontinued levothyroxine replacement therapy. Serum cholesterol and serum triglyceride levels increased in parallel, and classical type III hyperlipoproteinaemia (HLP) with xanthoma striata palmaris developed. The patient is homozygous for apolipoprotein (apo) E2. The case reported here represents the first example of manifestation of type III hyperlipoproteinaemia in a subject with secondary hypothyroidism bearing the apo E2/2 phenotype.     

老年痴呆患者apoE基因型分布

目的观察中国老年痴呆患者ａｐｏＥ基因型的分布，初步探讨ａｐｏＥ在老年痴呆发病中的作用。方法应用聚合酶链式反应（ＰＣＲ）对３５例健康人、２３例多梗塞性痴呆（ＭＩＤ）及１７例老年性痴呆（ＡＤ）患者进行ａｐｏＥ基因多态性分析，测定血清胆固醇（ＴＣ）、甘油三酯（ＴＧ）、高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）、低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）、载脂蛋白ＡⅠ（ａｐｏＡⅠ）、载脂蛋白Ｂ（ａｐｏＢ）和载脂蛋白Ｅ（ａｐｏＥ）的浓度。结果ＡＤ组与健康对照组在ａｐｏＥ基因频率及等位基因频率分布上的差异有显著性（χ２＝１１．５，Ｐ＜０．０５；χ２＝１６．２，Ｐ＜０．０１）；ＭＩＤ组与健康对照组间差异无显著性（Ｐ＞０．０５）；应用Ｗｏｏｌｆ公式计算，发现ａｐｏＥε４等位基因与ＡＤ之间有显著性关联（χ２＝７．７，Ｐ＜０．０１），相关危险度（ＲＲ）＝３．０。ＡＤ组血清ａｐｏＥ水平显著高于对照组（Ｐ＜０．０５），而ＴＣ、ＬＤＬ－Ｃ、ａｐｏＡⅠ、ａｐｏＢ显著低于对照组（Ｐ＜０．０５）。结论结果提示ａｐｏＥε４等位基因与老年性痴呆有显著性关联，ａｐｏＥε４可能是ＡＤ发病的危险因素。     

载脂蛋白B、E基因多态性与高血压病、冠心病的相关性研究

目的　探讨载脂蛋白 B、 E基因多态性与高血压、冠心病的相关性。方法　采用聚合酶链反应一限制性片段长度多态性分析 60例正常人、 60例高血压和 2 6例冠心病的载脂蛋白 B、E基因型。结果　高血压组和冠心病组的 Apo B的 Xba I位点等位基因频率高于正常组 ,其中冠心病组与正常组差异明显 ( P<0 .0 5 ) ,Apo E的等位基因 E4高于正常对照组 ( P<0 .0 5和 0 .0 0 5 )。结论　 Apo B的 Xba I位点和 Apo E的等位基因 E4是高血压和冠心病的重要遗传标记 ,推测该两种疾病的发生可能有共同的遗传基础     

载脂蛋白E及其基因变异在脂蛋白肾病发病中的作用

目的：研究载脂蛋白E（apoE)及其遗传变异在中国人脂蛋白肾病（LPG）发病中的作用。方法：收集本研究所收治的5例肾活检病理明确诊断的LPG患者,对临床资料进行分析;免疫比浊法检测血浆apoE水平,PCR－RFLP法研究apoE基因的遗传变异,结果：5例患者均以浮肿,尿检异常起病,肾功能正常,所有患者均伴有不同程度的贫血,低蛋白血症的和肾脏体积增大;血清甘油三酯水平显著增高,而总胆固醇正常或轻度增高,apoB,apoE水平也明显增高,而apoA-1正常;血清蛋白电泳显示α2,β-球蛋白增高,ApoE基因型分别为ε2/3,ε3/3,ε3/4, 另两患者为母子,RFLP图谱中均显示相同的异常条带,与apoE Tokyo型变异条带相似,结论：中国人LPG患者血清apoE水平明显升高,LPG患者存在apoE基因变异及基因型与表型不符合的现象。     

载脂蛋白E等位基因多态性与冠心病相关性的研究

对103例冠心病患者和100例正常对照者提取外周血白细胞DNA,采用PCR方法扩增apo E基因片段,经Hha I酶切,聚丙烯酰胺电泳分离,测得天津地区汉人apo R等位基分布,E4/3、E4/2、E3/3、E3/2在冠心病组和对照组基因频率分别为:0.068、0.019、0.854、0.058和0.060、0.010、0.800、0.130.E4/3基因型携带者胆固醇平均水平较高,E3/2基因型携带者甘油三酯平均水平较高.apo E基因多态性与冠脉受累数目无关.