PAI-1启动子区4G/5G基因多态性、ACE插入/缺失多态性与脑卒中的相关性

目的探讨纤溶酶原激活物抑制物-1(PAI-1)启动子区基因多态性和血管紧张素转换酶(ACE)插入/缺失多态性与脑卒中的关系。方法 PCR检测203例脑卒中患者和139名健康对照者PAI-1基因启动子区4G/5G多态性、ACE基因插入/缺失多态性,同时应用比色法测定血清ACE活性,发色底物法测定PAI-1活性。结果脑梗死(CI)组PAI-1活性(0.769±0.163 AU/mL)、ACE活性(43.42±14.36 U/L)明显高于对照组(0.652±0.116 AU/mL和31.28±8.64 U/L,P<0.01);CI组PAI-I基因4G纯合子、ACE D/I基因DD纯合子比例明显高于对照组(P<0.01);PAI-I基因4G/4G基因型与ACE基因D/D基因型对CI发病可相互协同作用(P<0.01)。结论 PAI-1基因4G/4G基因型和ACE基因D/D基因型均可能是CI发病的危险因素,且具有协同作用。     

妊娠期高血压孕妇血清中ACE水平及ACE基因16内含子I/D多态性分析

目的了解妊娠期高血压(gestationalhypertension,GH)孕妇血清中血管紧张素转换酶(Angiotensin ConvertingEnzyme,ACE)水平及ACE基因16内含子I/D多态性分布情况,并探讨其与深圳地区妊娠期高血压之间遗传基因易感性。方法收集2016年5月～2018年9月来医院产前检查并诊断为GH孕妇129例为GH组,选择同期产检的正常孕妇117名为对照组,采用AU5800全自动生化分析仪检测ACE水平,同时采用聚合酶链反应-限制性片段长度多态性(PCRRFLP)技术法对ACE基因16内含子I/D多态性进行分析,并对检测结果进行统计分析。结果 GH组血清中ACE水平为56.24±17.58U/L,明显高于对照组的34.82±11.09U/L,差异有统计学意义(t=3.0625,P0.05);GH组孕妇ACE基因16内含子I/DDD基因型及D等位基因频率分别为50.39%和62.02%,明显高于对照组孕妇的23.93%和31.20%,差异有统计学意义(χ2=3.0521～3.9745,P0.05);GH组DD基因型的孕妇血清中ACE水平为65.83±20.15U/L,略高于ID基因型的57.62±18.61U/L,差异无统计学意义(t=1.2054,P0.05),但明显高于II基因型的43.76±13.52U/L,差异有统计学意义(t=2.7162,P0.05)。结论 ACE水平在GH组孕妇血清中明显升高,同时ACE基因16内含子I/DDD基因型及D等位基因频率明显高于正常孕妇,且DD和ID基因型孕妇血清中ACE水平明显高于II基因型,可能是导致深圳地区孕妇GH发病的易感遗传基因之一。     

血管紧张素转换酶基因I/D多态性与血脂水平及原发性高血压的相关性探讨

目的 探讨血管紧张素转换酶(ACE)基因I/D多态性与血脂水平及原发性高血压（EH）的关系,为EH的病因学研究提供依据。方法 采用聚合酶链反应（PCR）对开滦煤矿汉族人群ACE基因Alu I/D多态性进行基因型检测。用全自动生化分析仪测定血清总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白（HDL）、低密度脂蛋白（LDL）含量。结果 调查人群中,HDL水平,携带ACE基因II基因型者高于携带ID、DD基因型者; LDL水平, 携带ID、DD基因型者高于携带II基因型者。EH组与非EH组比较,ACE基因不同基因型原发性高血压患病率不同, 携带ID(19.88%)、DD(20.82%)基因型者患病率高于携带II(14.26%)基因型者(P<0.05); ACE等位基因频率在两组间分布有差异（P<0.05,P<0.01）;除HDL含量和携带ID、II基因型者LDL含量外,其余血脂指标EH组与NEH组相比,各项均有差异（P<0.05）。在NEH组,TC水平,携带II基因型者高于携带DD基因型者;LDL水平,携带ID、DD基因型者高于携带II基因型者。结论 ACE基因不同基因型EH患病率不同,ACE基因I/D多态性与TC、HDL、LDL等血脂水平有关。     

对氧磷酶1 55 Met/Leu、对氧磷酶2 148 Ala/Gly基因多态性与冠状动脉粥样硬化性心脏病的关系

目的探讨对氧磷酶1 55Met/Leu(paraoxonase 1, PON1 55Met/Leu)、对氧磷酶2 148 Ala/Gly(PON2148 Ala/Gly)基因多态性与冠状动脉粥样硬化性心脏病(简称冠心病)、血浆对氧磷酶(paraoxonase,PON)、总超氧化物歧化酶(total superoxide dismutase, T-SOD)活性以及丙二醛(maleic dialdehyde, MDA)浓度的关系.方法采用聚合酶链反应-限制性片段长度多态性方法检测262例冠心病患者和100名对照的PON1 55Met/Leu、PON2 148 Ala/Gly基因多态性,采用比色法测定血浆PON、T-SOD活性以及MDA浓度.结果与对照比较,冠心病患者的血浆PON[(349.27±138.36) nmol/min· mL vs. (454.75±166.00) nmol/min*mL, P<0.01]、T-SOD[(23.61±16.51) U/mL vs. (44.01±22.68) U/mL, P<0.01]活性明显降低,MDA浓度显著增高[(2.47±0.73) nmol/mL vs. (2.15±0.55) nmol/mL, P<0.01];冠心病患者的PON1 55 LM杂合子基因型(24.8% vs. 1.4%, P<0.01)、M等位基因频率(12.4% vs. 0.5%,P=0.001),PON2148 GG纯合子基因型和AG 杂合子基因型(11.8% vs. 5.0%和48.1% vs. 24.0%, P<0.01)、G等位基因频率(36.0% vs. 17.0%, P<0.01)较对照组明显增高;PON1 55 LM杂合子基因型的PON和T-SOD活性较LL纯合子基因型明显降低(P<0.01和P<0.05);PON2148 GG基因型和AG基因型的PON活性较AA基因型明显降低(P<0.01);Logistic回归分析显示PON1 55 LM杂合子基因型、M等位基因、PON2 148GG/AG基因型、G等位基因是冠心病的危险因子.结论冠心病患者的血浆PON和T-SOD活性明显降低,MDA浓度显著增高;PON1 55Met/Leu的LM基因型和M等位基因、PON2148 Ala/Gly的GG/AG基因型和G等位基因是冠心病的危险因子,并且与其他基因型相比,这些基因型患者的血浆PON活性降低.     

内皮素和一氧化氮/一氧化氮酶检测对老年糖尿病与血管病变患者临床价值的研究

探讨内皮素(ET)、一氧化氮/一氧化氮酶( NO/NOS)在糖尿病与血管病变患者中的变化。ET采用放射免疫分析法,NO/NOS采用酶法。结果是:(1)糖尿病组ET水平(68.80±37.35)pg/mL)较对照组(41.70±21.50pg/mL)显著升高(P<0.001);NOS水平(2.75±1.49U/mL)明显高于对照组(1.12±0.56U/mL),P<0.01;NO水平(49.32± 16.32μmol/L)明显低于对照组(54.60 ±15.60μmol/L),P<0.05。(2)糖尿病合并血管病变组ET水(80.1140.25pg/mL)显著高于无并发症组(62.73±24.29pg/mL),P<0.001;NOS水平(4.02 ± 0.59U/mL)明显高于无并发症组(2.51±1.19U/mL),P<0.001;NO水平(42.25 ± 10.10/μmol/L)明显低于无并发症组(52.16±14.59mol/L,P<0.05;NO/NOS(11.99±7.05)明显低于无并发症组(26.9±13.15),P<0.001提示 ET、NO/NOS与糖尿病的发生和发展有关,联合检测不仅可作为糖尿病及其血管并发症的重要依据,还将有助于糖尿病合并血管病变的预防和治疗。     

血清胞苷脱氨酶在活动性类风湿关节炎诊疗中的意义

目的:探讨测定血清胞苷脱氨酶(CD)含量对活动性类风湿关节炎(RA)患者的诊疗价值。方法:采用分光光度法测定血清中的胞苷脱氨酶活性,同时用免疫比浊法测定C反应蛋白(CRP),魏氏法测定血沉(ESR)。结果:活动性RA组血清CD含量(14.80±2.11)U/m l,显著高于正常对照组(4.86±1.86)U/m l,(P<0.01);CRP(51.46±20.43)mg/L和ESR(85.03±27.6)mm/1h明显高于正常对照组(3.40±2.21)mg/L,(13.04±4.89)mm/1h(均P<0.01);活动性RA患者组CD含量与ESR、CRP成直线关系,相关系数r分别为0.6324(P<0.01)与0.8013(P<0.01)。结论:血清CD活性可作为活动性RA患者急性感染的早期诊断指标,对活动性RA患者的预后判断亦有临床价值。     

肾综合征出血热患者血浆和血清可溶性IL-2R水平变化的研究

本文应用双McAb ELISA夹心法检测了HFRS患者血清和血浆中SIL-2R水平。结果表明,急性期患者血浆和血清中sIL-2R水平(分别为199±81U/ml和214±122U/ml)显著地高于恢复期患者(分别为104±37U/ml和97±28U/ml)和正常人(分别为88±31U/ml和71±21U/ml)(P<0.01);在急性期中尤以少尿期升高最明显。表明HFRS患者机体免疫细胞处于高度活化的状态,患者血清和血浆中sIL-2R的检测对于判断病期和指导治疗均有一定的意义。     

新的心肌梗塞危险因素

与心脏病致病因素不同,心肌梗塞(MI)的危险因素可能与血管紧张素转换酶(ACE)基因,多形核白细胞减少有关。这一证据来自多中心的研究,在610例MI患者中发现DD基因型(全身ACE的浓度要比ID或Ⅱ基因型高)出现的机率要比对照组733例高(P=0.007)。前3种基因类型中患者对血浆脂体易变性、纤维蛋白原、机体指数(body-Mass index),吸烟量、血压或高血压的个体之间无明显差异。此外,低危险组的病人中DD基因型和MI之间有显著相关意义(P<0.001)。因此,作者认为对这一结果有     

乙型肝炎病毒基因型不同的患者肝功能相关指标及免疫功能变化分析

目的 探讨基因型不同的乙肝患者肝功能、病毒载量和免疫功能的差异及临床意义.方法 145例乙肝患者划分两个年龄段:小于35岁和大于35岁,全部应用实时荧光PCR法进行乙型肝炎病毒(HBV)基因分型检测;同时采用实时荧光PCR法检测血清HBV-DNA载量;用全自动生化分析仪和流式细胞仪检测各组肝功能相关指标及淋巴细胞亚群含量.结果 145例HBV患者仅为两种基因型,B基因型62例(42.76％),C基因型83例(57.24％).B型患者谷丙转氨酶(ALT)、谷草转氨酶(AST)和HBV-DNA均稍高于C型,分别是[(263.6±36.13) U/L比(243.1±37.69) U/L]、[(128.1±15.84) U/L比(123.6±19.1)U/L]和[(6.131±0.2133)比(5.875±0.1725)],进行统计学分析后差异均无统计学意义(P＞0.05),但划分年龄段后,大于35岁的患者,B型ALT、AST和HBV-DNA均显著高于C型(P＜0.05),分别是[(227.6±34.52) U/L比(144.8±19.92) U/L]、[(124.5±19.4) U/L比(79.79±12)U/L]和[(6.166±0.2582)比(5.228±0.2644)].淋巴细胞亚群分析可见,所有年龄段或大于35岁患者均是B型的CD4+T细胞比例显著低于C型[(32.97±0.95)％比(35.81±0.85)％](P＜0.05),CD8+T细胞显著高于C型[(30.19 ±0.97)％比(27.44±0.92)％](P＜0.05),而CD3+T细胞、B细胞、NK细胞在B型和C型患者中则差异无统计学意义(P＞0.05).结论 145例HBV患者B、C型的分布未见显著差异;肝功能、病毒载量及T细胞亚群在年龄较大的B、C两组患者中存在显著差异.     

P-糖蛋白单克隆抗体改善MRL/lpr狼疮鼠肾脏病变的研究

目的 探讨P-糖蛋白(P-glyeoprotein,P-gp)单克隆抗体(UIC2)在改善MRL/lpr狼疮鼠肾脏病变中的作用.方法 24只14周龄雌性MRl/lpr狼疮鼠分为3组:P-gp单克隆抗体1次治疗组(G1)、P-gp单克隆抗体3次治疗组(G2)、对照组(G0).观察体重;采用考马斯亮蓝法检测24 h尿蛋白定量;采用酶联免疫吸附法试验(enzyme linked immunosorbent assay,ELISA)检测抗双链DNA(dsDNA)抗体水平;采用酶法检测血清肌酐水平;采用苏木素-伊红染色、免疫荧光和电镜观察肾脏病理改变.结果 ①22周时G1组和G2组体重高于G0组(P<0.05).② 24 h尿蛋白定量22周时Gl组[(1.9±1.1)mg]和G2组[(1.4±0.9)mg]低于G0组[(3.1±1.9)mg](P<0.05);26周时G1组[(2.4±1.4)mg]和G2组[(1.8±1.1)mg]低于G0组[(5.3±2.2)mg](P<0.05).③26周时血清肌酐G1组[(7.0±2.9)μmol/L]和G2组[(6.1±2.5)μmol/L]低于G0组[(12.7±1.3)umol/L](P<0.05).④19周时,抗dsDNA抗体滴度G1组[(43±19)×102 U/mL]和G2组[(45±32)×102 U/mL]低于G0组[(87±39)×102 U/mL](P<0.05);26周时G2组[(35±11)×102 U/mL]低于G0组[(59±35)×102 U/mL].⑤肾小球新月体形成率G1组(0.11±0.05)和G2组(0.09土0.01)低于G0组(0.23±0.07),G2组较Gl组减低(P均<0.05).结论 P-gp单克隆抗体可改善MRl/lpr狼疮鼠肾脏病变的进展,减少尿蛋白、降低血清肌酐,对狼疮肾炎有显著疗效.     

PAI-1启动子区4G/5G基因多态性、ACE插入/缺失多态性与脑卒中的相关性

目的 探讨纤溶酶原激活物抑制物-1(PAI-1)启动子区基因多态性和血管紧张素转换酶(ACE)插入/缺失多态性与脑卒中的关系.方法 PCR检测203例脑卒中患者和139名健康对照者PAI-1基因启动子区4G/5G多态性、ACE基因插入/缺失多态性,同时应用比色法测定血清ACE活性,发色底物法测定PAI-1活性.结果 脑...     

The angiotensin converting enzyme genetic polymorphism in acute coronary syndrome--ACE polymorphism as a risk factor of acute coronary syndrome.

The deletion polymorphism of angiotensin converting enzyme (ACE) genotype has been reported as an independent risk factor for the development of myocardial infarction (MI). However there are conflicting data showing no relationship between the ACE genotype and coronary artery disease. The present study was performed to investigate the correlation between ACE genetic polymorphism and acute coronary syndrome by comparing the distribution of ACE genotypes and ACE activities in patients with acute MI and unstable angina with those in control group. The frequency of genotype DD was significantly higher in patients with acute coronary syndrome than in controls. Logistic regression analysis showed that ACE polymorphism affected the development of acute coronary syndrome in recessive pattern of D allele. When we divided the patients into MI and unstable angina groups, the frequencies of genotype DD and D allele were significantly higher in unstable angina group than in MI or control groups. In the patients with MI, the frequency of D allele was significantly higher in patients without previous angina than in those with previous angina. There was no significant difference in ACE genotype or allelic frequency according to the severity of coronary lesions. The ACE genotype was associated with marked differences of ACE activity, but there was no difference between the patient and control groups for each genotype. In conclusion, the genotype DD of ACE gene associated with acute coronary syndrome, but not with the severity of coronary artery lesion. These results showed that the genotype DD of ACE gene might be associated with acute coronary syndrome by another mechanism rather than the coronary atherosclerosis.     

Plasminogen activator inhibitor-1 C/G polymorphism in relation to plasma levels in rheumatoid arthritis

Plasminogen activator inhibitor type 1 (PAI-1) is an inhibitor of plasmin production. Plasmin can directly or indirectly to degrade cartilage and bone matrix. The PAI-1 HindIII polymorphism has been associated with high PAI-1 plasma levels in myocardial infarction patients and control populations. Furthermore, it has been associated with the angiographic extent of coronary artery disease, but their involvement in other diseases is still uncertain. Here, we assessed the relationship between PAI-1 HindIII polymorphism and PAI-1 plasma levels in rheumatoid arthritis (RA). One hundred and twenty-five RA patients and 132 control subjects (CS) were included. Genotypes were identified by the polymerase chain reaction-restriction fragment length polymorphism technique and PAI-1 plasma levels were quantified using an ELISA kit. Not significant differences in genotype and allele frequencies between both studied groups were observed (P > 0.05). RA patients showed lower PAI-1 plasma levels (18.92 ± 12.94 ng/ml) than CS (23.68 ± 23.38 ng/ml), without significant difference (P = 0.299). However, in RA patients the C/G genotype carriers showed higher PAI-1 plasma levels (23.00 ± 13.81 ng/ml) with respect to C/C (16.77 ± 11.97 ng/ml) and G/G (10.47 ± 7.07 ng/ml) genotype carriers (P = 0.036). The PAI-1 HindIII polymorphism was not associated with RA susceptibility. However, the C/G genotype is associated with high PAI-1 plasma levels in RA patients.     

The serum angiotensin-converting enzyme and angiotensin II response to altered posture and acute exercise, and the influence of ACE genotype

The deletion (D) rather than insertion (I) allele of the angiotensin-converting enzyme (ACE) gene is associated with greater ACE activity. We examined: (1) the influence of posture change (recumbent to seated) and acute exercise on serum ACE and angiotensin II (Ang II) activity; (2) the relationship between ACE and Ang II levels; and (3) the influence of ACE genotype on changes in ACE and Ang II levels with posture and exercise. Recreationally active young male Caucasians (10 each of II, ID and DD genotypes) rested for 35 min supine then 15 min upright, took 20 min bicycle ergometric exercise at 70% maximum oxygen uptake, then rested for 40 min. Samples were taken throughout for ACE activity and Ang II levels. Supine ACE levels were dependent upon ACE genotype [24.8 (5.7), 26.9 (4.5), 45.5 (6.4) nmol His-Leu ml^–1 min^–1; II, ID, DD, respectively; P<0.00005] and thereafter. ACE activity rose with assumption of a seated posture [from 32.4 (10.9) nmol His-Leu ml^–1 min^–1 to 35.0 (11.5) nmol His-Leu ml^–1 min^–1, P<0.00001], the absolute rise being independent of genotype [3.22 (1.92), 1.6 (1.6), 2.4 (2.3) nmol His-Leu ml^–1 min^–1; II, ID, DD; P=0.22], unlike percentage change [12.8 (6.8), 5.6 (5.5), 5.3 (5.0)%; II, ID, DD; P<0.01, and P=0.004 for II vs presence of the D allele]. A further genotype-independent rise occurred with exercise [+2.9 (3.7) units, P<0.0003]. An associated rise in Ang II levels [30.3 (15.9), or 2587.9 (489.76)%, P<0.00001] was independent of ACE genotype or activity. Upright posture increases ACE activity, and this may be influenced by ACE genotype. ACE activity and Ang II levels rise independently with exercise in a non-genotype-dependent fashion.     

ACE/DD基因型和MYH7突变与原发性高血压左室肥厚的关系

 目的 探讨ACE/DD基因型与MYH7突变联合作用和高血压左室肥厚（LVH）的关系。方法 对102例高血压LVH患者与101例高血压非LVH患者以及100例正常对照进行病例-对照研究。超声心动图测量和计算左室重量指数（LVMI）。用聚合酶链反应（PCR）、限制性片段长度多态性（RFLP）检测ACE/ID多态性,双脱氧末端测序方法检测MYH7基因突变。结果 高血压LVH组ACE基因DD基因型频率显著高于高血压非LVH组和正常对照组（P<0.01）;MYH7基因未发现突变。结论 ACE基因多态性与高血压LVH形成有关,DD基因型易发生左心室肥厚。MYH7基因突变与高血压LVH无明显关系,ACE基因DD基因型与MYH7基因间不存在联合作用。     

类风湿性关节炎患者血清中自身抗体ACⅡ、ACCP检测的价值

目的 探讨类风湿性关节炎患者血清中自身抗体ACⅡ、ACCP检测的价值.方法 收集2014年2月至2016年3月于我院风湿科住院的类风湿关节炎患者106例作为类风湿关节炎组,同期选择在我院进行体检的健康者106例作为对照组,两组都进行ACⅡ、ACCP、RF的检测与阳性率判断和相关性分析.结果 类风湿性关节炎组的血清ACCP、ACⅡ、RF水平分别为15.93±1.44 U/mL、30.22±7.14 U/mL和28.93±4.29 IU/mL,都明显高于对照组的2.78±0.99、5.11±2.84、10.93±5.33(P<0.05).类风湿性关节炎组血清ACCP、ACⅡ、RF阳性率分别为71.7%、61.3%和70.0%,都明显高于对照组的0.0%、0.0%和5.7%(P<0.05).在类风湿性关节炎组中,Pearson相关性检验显示ACCP、ACⅡ与RF都呈明显正相关性(P<0.05).结论 类风湿性关节炎患者血清中自身抗体ACⅡ、ACCP都呈现高表达状况,且与患者的风湿因子表达呈现正相关性,有很好的临床诊断与鉴别价值.     

Omega-3 fatty acid improves the clinical outcome of hepatectomized patients with hepatitis B virus(HBV)-associated hepatocellular carcinoma

Omega-3 fatty acid supplemented total parenteral nutrition improves the clinical outcome of patients undergoing certain operations;however,its benefits for patients with hepatitis type B virus(HBV)-associated hepatocellular carcinoma(HCC) who have undergone hepatectomy are still not clear.The aim of this study was to evaluate the effect of omega-3 fatty acid supplemented total parenteral nutrition on the clinical outcome of patients with HBV-associated HCC who underwent hepatectomy at our institution.A total of 63 patients with HBV-associated HCC who underwent hepatectomy were included in this study.These patients were randomly assigned to receive stand-ard total parenteral nutrition(the control group,n = 31) or omega-3 fatty acid supplemented total parenteral nutri-tion(the omega-3 fatty acid group,n = 32) for at least 5 d.The study endpoints were the occurrence of infection-related complications,recovery of liver function and length of hospital stay.The results showed that the omega-3 fatty acid group had a lower infection rate(omega-3 fatty acid,19.4% vs control,43.8%,P < 0.05),a better liver function after hepatectomy:alanine transaminase(omega-3 fatty acid,48.23±18.48 U/L vs control,73.34±40.60 U/L,P < 0.01),aspartate transaminase(omega-3 fatty acid,35.77±14.56 U/L vs control,50.53±24.62 U/L,P < 0.01),total bilirubin(omega-3 fatty acid,24.29±7.40 mmol/L vs control,28.37±8.06 mmol/L,P < 0.05) and a shorter length of hospital stay(omega-3 fatty acid,12.71±2.58 d vs control,15.91±3.23 d,P < 0.01).The serum contents of IL-6(omega-3 fatty acid,23.98±5.63 pg/mL vs control,35.55±7.5 pg/mL,P < 0.01) and TNF-α(ome-ga-3 fatty acid,4.43±1.22 pg/mL vs control,5.96±1.58 pg/mL,P < 0.01) after hepatectomy were significantly lower in the omega-3 fatty acid group than those of the control group.In conclusion,administration of omega-3 fatty acid may reduce infection rate and improve liver function recovery in HBV-associated HCC patients after hepatectomy.This improvement is associated with suppressed production of proinflammatory cytokines in these patients.     

丝瓜降血脂及抗氧化作用的实验研究

目的： 观察丝瓜（LC）多酚的抗氧化作用及丝瓜对实验性高脂血症小鼠的影响。方法: 利用丙酮提取丝瓜多酚类物质，用福林法测定其含量并观察丝瓜多酚粗提液抑制羟自由基生成的能力。用高脂饲料喂养昆明小鼠建立高脂血症模型，以血脂康作为阳性对照观察饲料中补充丝瓜冻干品喂养对小鼠血清胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白（LDL-C）、超氧化物歧化酶（SOD）及肝组织中丙二醛（MDA）的影响。结果: （1）新鲜丝瓜多酚含量为0.3 g/kg±0.1 g/kg。（2）新鲜丝瓜多酚粗提液具有较强的抑制羟自由基生成的能力。(3)与高脂模型组比较，低剂量丝瓜组、高剂量丝瓜组小鼠体重增加趋势明显减轻。(4)低剂量丝瓜组TC（4.19±0.37）mmol/L和LDL-C（2.77±0.79）mmol/L、高剂量丝瓜组TC（3.56±0.55）mmol/L和LDL（2.34±0.41）mmol/L、血脂康阳性对照组TC（4.59±0.96）mmol/L和LDL-C（3.25±0.67）mmol/L均低于高脂模型组TC(7.20±0.87)mmol/L和LDL-C(4.92±0.52)mmol/L（P＜0.01），其中高剂量丝瓜组TC、LDL-C下降最为明显。(5)低剂量丝瓜组和高剂量丝瓜组小鼠血清SOD分别为（337.00±29.73） U/mL和(349.00±9.99)U/mL，均高于高脂模型组和空白对照组，其中高剂量丝瓜组SOD活性明显高于高脂模型组（P＜0.01）。结论: 丝瓜多酚具有较强的抗氧化作用，丝瓜能明显降低高脂血症小鼠的体重、肝指数及血脂水平。     

硝基酪氨酸和诱导型一氧化氮合酶在大鼠胎粪吸入性肺损伤中表达的研究

目的：观察大鼠胎粪诱导肺损伤时肺组织硝基化酪氨酸和诱导型一氧化氮合酶（iNOS）表达的改变，探讨两者在此种损伤中的作用。 方法： 16只雄性SD大鼠，随机分为对照组和胎粪组，分别由气管插管注入生理盐水或20%胎粪生理盐水混悬液1 mL/kg。24 h后取材，观察支气管肺泡灌洗液（BALF）细胞计数，比色法检测肺组织匀浆髓过氧化物酶（MPO）活性、一氧化氮（NO）含量，Western blot法测定硝基酪氨酸和iNOS蛋白表达改变。 结果： 胎粪组BALF细胞计数、肺组织MPO活性、NO含量分别为(4.04±1.01)×109cells/L、(1.49±0.22)U/g wet lung tissue、(12.77±5.00)mmol/g protein，对照组BALF细胞计数、肺组织MPO活性、NO含量分别为(0.53±0.19)×109cells/L、(0.62±0.16)U/g wet lung tissue、(4.89±1.32)mmol/g protein，两组比较差异显著（均P<0.01）；Western blot结果显示胎粪组肺组织硝基酪氨酸和iNOS蛋白表达明显强于对照组，分别为0.46±0.19和1.49±0.60，与对照组（0.15±0.04和0.09±0.04）比较, 差异显著（均P<0.01）。 结论： 胎粪可诱导iNOS表达增强并产生过量的硝基酪氨酸，两者可能在胎粪性肺损伤发病机制中发挥重要作用。