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电针丰隆对高脂血症模型大鼠胆固醇逆转运通路的影响
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摘要
目的
     高脂血症是指机体内脂肪代谢或转运异常所致。大量的流行病学调查和研究均表明,高脂血症是动脉粥样硬化、高血压、冠心病、糖尿病等多种疾病发生的重要危险因素。近几年非药物疗法治疗高脂血症受到重视,尤其是临床应用针刺疗法治疗高脂血症,有了较大的进展,疗效也较为显著,显示出独特的优势。本实验旨在以高脂血症大鼠模型为研究对象,以胆固醇逆转运通路为切入点,观察各组大鼠血脂水平、血液流变学、巨噬细胞炎症因子、肝脏和主动脉弓组织形态学变化及ABCA1、SR-BI、PPAR Y、IGF-1的基因、蛋白表达,探讨电针丰隆穴对胆固醇逆转运通路的影响以及防治高脂血症的作用机制。
     方法
     选取成年雄性大鼠40只,适应性喂养1周后,将实验大鼠随机分空白对照组、模型+普通饲料组、模型+高脂饲料电针组、模型+普通饲料电针组这4组,每组10只。治疗结束后,将各组大鼠经颈动脉取血,测定血脂(TC、TG、HDL-C、LDL-C)含量及血液流变学指标(全血高切相对指数、全血低切相对指数、血浆黏度、红细胞聚集指数)。然后分离各组大鼠腹腔巨噬细胞,加荧光标记的炎症因子分子抗体后应用流式细胞仪检测ICAM-1、MCP-1、TNF-α、IL-6的含量。用HE染色法,在光镜下观察各组大鼠肝脏组织和主动脉弓组织形态学变化情况。检测肝脏组织ABCA1、 SR-BI、PPARγ、IGF-1的基因(mRNA)表达影响和蛋白含量。
     结果
     ①与空白对照组相比较,其余三组血清TC值均显著上升,有非常显著性差异(P<0.01)。模型+普通饲料组和模型+高脂饲料电针组与空白对照组比较血清LDL-C值显著上升,差异具有非常显著性(P<0.01),而HDL-C值明显下降,差异具有显著性(P<0.05)。与模型+普通饲料组相比较,模型+高脂饲料电针组和模型+普通饲料电针组血清TC、LDL-C值均显著降低,有非常显著性差异(P<0.01)。②除模型+普通饲料电针组外,其余各组大鼠血液流变学(全血高切相对指数、全血低切相对指数、血浆黏度、红细胞聚集指数)与空白对照组比较均有所增加,具有显著型差异(P<0.05,或P<0.01);与模型+普通饲料组比较,模型+普通饲料电针组大鼠血液流变学各项指标均有明显下降,有非常显著性差异(P<0.01)。③除模型+普通饲料电针组组外,其余各组大鼠腹腔巨噬细胞内ICAM-1、 MCP-1、TNF-a、IL-6与空白对照组比较均有明显升高(P<0.01,P<0.05)。与模型+普通饲料组比较,模型+普通饲料电针组的IL-6有明显减少(P<0.05), ICAM-1、MCP-1、TNF-a均显著减少,两组比较具有非常显著性差异(P<0.01)。④模型+普通饲料组大鼠肝脏组织可见中度到重度弥漫性脂肪变性,肝脏组织已经出现损害,有脂肪沉积情况。主动脉弓动脉管壁厚薄不均,内膜增厚和脂质沉着,主动脉内皮细胞严重破坏,内膜不连续,大量的泡沫细胞沉积于内膜下层,可见病变脂纹脂斑。而高脂造模成功后给予针刺治疗同时分别加高脂饲料、普通始料喂养的两组情况有不同程度改善,肝脏组织病变程度有所减轻,肝细胞结构部分修复,脂肪沉积减轻,主动脉弓组织血管壁结构有所修复清晰,内皮下脂质及炎性细胞浸润减少,中膜弹力膜有所修复。⑤与空白对照组比较,除了模型+普通饲料电针组外,其余两组ABCA1、SR-BI、PPARγ均有显著降低(P<0.01),IGF-1有显著升高(P<0.01);与模型+普通饲料组比较,模型+高脂饲料电针组只有SR-BI和IGF-1这两个数值有差异性(P<0.05),而模型+普通饲料电针组的ABCA1、SR-BI、PPARγ均有显著降低(P<0.01), IGF-1有显著升高(P<0.01);与模型+高脂饲料电针组比较,模型+普通饲料电针组的ABCA1、SR-BI、PPAR γ、IGF-1均有显著差异性(P<0.05,P<0.01)。
     结论
     电针丰隆穴能降低高脂血症大鼠TC、LDL-C水平,升高HDL-C水平,改善高脂状态下血液浓、黏、聚、凝的高危险状态,减少大鼠巨噬细胞内炎症因子ICAM、MCP-1、TNF-a、IL-6的含量,改善大鼠肝脏及主动脉弓形态学变化,有效抑制脂肪变性的发生程度,清除脂肪细胞,保护血管内皮,减少脂质沉积,对于动脉硬化早期的血管壁具有一定的保护作用。电针丰隆穴通过提高胆固醇逆转运通路两个重要功能蛋白ABCA1、SR-BI的表达,加速脂质代谢,达到治疗高脂血症的目的。
Objective:
     Hyperlipidemia refers to the abnormality in the body fat metabolism or transporter. A large number of epidemiological surveysthat hyperlipidemia is an important risk factor for atherosclerosis, high blood pressure, coronary artery disease. In recent years, non-drug therapy for hyperlipidemia attention, especially the clinical appl i cat ion of acupuncture in the treatment of hyperlipidemia, has made significant progress, the effects are more significant, showing a unique advantage. The purpose of this experiment is to hyperlipidemia rat model for the study of reverse cholesterol transport pathway as an entry point to observe the rats in each group lipid levels, hemorheology, macrophage inflammatory factor, liver and aortic arch tissue morphology. changes ABCA1, SR-BI, PPARγ, IGF-1gene and protein expression, electro-acupuncture the Fenglong on reverse cholesterol transport pathway the prevention and control of the mechanism of action of hyperlipidemia.
     Methods:
     Select40adult male SD rats, after adaptive feeding for1week, the rats were randomly divided into blank control group, model+normal diet group, model+high fat diet EA group, model+normal diet EA group. Each one has ten rats. After the end of treatment, the rats in each group through carotid artery blood, serum lipids (TC, TG, HDL-C, LDL-C) content and blood rheology indicators (high shear blood relative index, whole blood low shear relative index, plasma viscosity, erythrocyte aggregation index). Peritoneal macrophages of rats in each group were then separated and analyzed by flow cytometry plus fluorescently labeled antibody inflammatory cytokines molecules ICAM-1, MCP-1, TNF-α, IL-6levels. HE staining, is aim to observe the tissue morphological changes of the the rats liver tissue and the aortic arch in the light microscope. Detection of liver tissue of ABCA1and SR-BI, PPAR y, IGF-1gene (mRNA) expression and protein content.
     Results:
     ①The with blank control group relative comparison, the remaining three groups plasma TC values are significant with the rise, there are very significant with difference (P<0.01), model+ordinary feed group and model+high-fat feed electric acupuncture group plasma LDL-C values significantly with the rise, the difference has very significantly with sex (P<0.01), HDL-C values significantly decreased, significant sex (P<0.05) difference; model+ordinary feed group phase comparison model+high-fat feed EA group and model+normal diet EA plasma TC, LDL-C values were significantly reduced, and there was a significant difference (P<0.01).(2) In addition to the model+EA group beginning material remaining rats hemorheology (whole blood high shear relative index of whole blood relative index, plasma viscosity, erythrocyte aggregation index) compared with the blank control group, both an increase in type differences (P<0.05, P<0.01); model+common starting material group Hemorheology model+normal diet EA group was significantly decreased (P<0.01).③In addition to the model+normal diet EA group group, the rest of the rats in each group peritoneal macrophages ICAM-1, MCP-1, TNF-a, IL-6compared with the blank control group were significantly increased (P<0.01, P<0.05). Compared with the model+ordinary feed group model+feed electric needle group in addition of IL-6have decreased significantly (P <0.05), the expression of ICAM-1, MCP-1, of TNF-a were very significantly with the decline, with a significant differences (P <0.01).④model+normal diet group rat liver tissue visible moderate to severe diffuse fatty degeneration of the liver tissue damage and fat deposition. The arterial wall of the aortic arch uneven thickness, intimal thickening and lipid calm, severely damaged aortic endothelial cells, endometrial discontinuous foam cells are deposited in the intima lower spot visible lesions fatty streaks fat. Given acupuncture treatment of hyperlipidemia successful modeling and high fat diet, the ordinary start feeding feeding two sets of circumstances are different degrees of improvement, the severity of liver tissue has been reduced, the structural part of the repair of liver cells, reduce fat deposition, aortic arch organizations vessel wall structure was repaired clear, reduce of subendothelial lipid and inflammatory cell infiltration, membrane stretch film some repair.⑤with blank control group, model+normal diet EA group, and the remaining two groups of ABCA1and SR-BI of PPARγ were significantly lower (P<0.01), and IGF-1significantly increased (P<0.01); model+normal diet group compared with the model+high fat diet EA group only SR-BI and IGF-1two numerical differences (P<0.05), while the model+normal diet EA group ABCA1, SR-BI, PPAR y were significantly (P<0.01) reduction in IGF-1significantly increased (P<0.01); model+high fat diet EA group, model+normal diet EA group ABCA1, SR-BI, PPAR Y, IGF-1were significant differences (P<0.05, P<0.01).
     Conclusion:
     EA Fenglong reduce hyperlipidemia rats TC, LDL-C levels, increased HDL-C levels, improve blood concentration in high-fat state, sticky, poly, condensate at high risk status, reduce macrophage inflammatory cytokines of ICAM, MCP-1, TNF-a and IL-6, improve rat liver and aortic arch morphological changes effectively suppress the occurrence of steatosis remove fat cells protect vascular endothelial reduce fatsedimentary, early atherosclerosis vascular wall has a protective effect. Electro-acupuncture the Fenglong by elevate cholesterol reverse transport the path two important functional protein of ABCA1and SR-BI expression, accelerated lipid metabolism, to achieve the purpose of the treatment of hyperlipidemia.
引文
[1]血脂治疗现状调查协作组.我国血脂异常治疗现状的调查[J].中华心血管病杂志,2001,29(1):15-18.
    [2]张唐法,万文俊,张红星,等.电针丰隆穴治疗高脂血症的多中心观察[J].中国临床康复2006;10(9):17-19
    [3]吕建敏,应华忠,徐孝平,等.高脂血症动物模型研究进展[J].浙江中医学院学报,2005,29(4):87-89.
    [4]王琼,乐薇,覃鹏飞,等.三种高脂血症实验性大鼠模型的比较[J].中国康复,2010,25(5):330-331.
    [5]倪鸿昌,李俊,金涌等.大鼠实验性高脂血症和高脂血症性脂肪肝模型研究[J].中国药理学通报,2004;20(6):703-705
    [6]Fernandez ML, WilSon TA, Conde K, et al. Hamsters and guinea pigs differIn their plasma lipoprotein cholesterol distribution when fed diets varying in animal protein, soluble fiber or cholesterol content. J Nutr,1999:129 (7):13-23.
    [7]Kris-Etherton PM and Diteschy J. Design criteria for studies examining individual fatty acid effects on cardiovaseular disease risk factors:human and animal studies. Am J Clin Nutr, 1997;65(supp 1):1594-1595.
    [8]陈凯,张雁芳,王倩,等.高胆固醇饲养兔鹤鹑和大鼠诱发高血脂和动脉粥样硬化的特征.解放军药学学报(J),2001,117-124.
    [9]Boehler, N.et al. Antilithiasic effect of beta-cyclodextrin in LPN hamster:comparison with cholestyramine. J Lipid Res,1999, 40:726-734
    [10]高莹,李可基,唐世英,等.几种高脂血症动物模型的比较[J].卫生研究,2002,31(2):97-99.
    [11]张红星,王琼,乐薇,等.高脂血症大鼠模型建立的动态研究[J].湖北中医药大学学报.2010,13(1):19-22.
    [12]刘嵩,卢笑丛,葛建,等.高脂所致脂肪肝动物模型建立的动态研究[J].中国药理学通报.2006,22(11):1399-1402.
    [13]Balbisi EA. Management of hyperliPidemia:new LDL-C targets for Persons at high-risk for cardiovascular events. Med Sci Monit2006:12(2):34-39
    [14]陆再英,钟南山.内科学[M].北京:人民卫生出版社.2008:267-274.
    [15]孟晓萍,布艾加尔·哈斯木.动脉粥样硬化[M].北京:人民卫生出版社.2011:377-415
    [16]Scandinavian Simvastatin Survival Study Group:Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease:the Scandinavian Simvastatin Survival tudy(4S). Lancet,1994; 344:1383-1389.
    [17]Shepherd J, Cobbe SM, Ford I,et al. For the West of Scotland Coronary Prevention Stuty Group:Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med,1995; 333:1301-1307.
    [18]Glass CK, Witztum JL. Atherosclerosis. the roed ahead. Cell, 2001; 104:503-516.
    [1]吕建敏,应华忠,徐孝平,等.高脂血症动物模型研究进展[J].浙江中医学院学报,2005,29(4):87-89.
    [2]王琼,乐薇,覃鹏飞,等.三种高脂血症实验性大鼠模型的比较[J].中国康复,2010,25(5):330-331.
    [3]陈可翼.活血化瘀研究与临床[M].中国协和医科大学联合出版社1993,13-18
    [4]余林中.温病微观的证治[J].中医研究.1996,9(5):4-5
    [5]刘景泉,王淑萍,苏海,等.高脂血症患者血液流变学指标检测[J].中国医学理论与实践,2005,15(12):15-18
    [6]田庆印,吴葆杰.氧化型低密度脂蛋白与血栓形成[J].中国动脉硬化杂志,2000,8(3):279-282
    [7]刑文革,朱文云,马丽,等.高脂血症血流变与细胞流变性变化机理的研究[J].微循环杂志,2001,11(2):27-29
    [8]刘志军,赵淑青.血脂异常对纤溶功能影响的研究[J].医学综述,2002,8(8):474-475
    [9]刘素蓉.痰浊之血与血液流变学相关性研究[J].实用中西结合杂志,1996,9(5):28-30
    [1]孟晓萍,布艾加尔·哈斯木.动脉粥样硬化[M].北京:人民卫生出版社.2011:377-415
    [2]吕建敏,应华忠,徐孝平,等.高脂血症动物模型研究进展[J].浙江中医学院学报,2005,29(4):87-89.
    [3]王琼,乐薇,覃鹏飞,等.三种高脂血症实验性大鼠模型的比较[J].中国康复,2010,25(5):330-331.
    [4]兰青,尹美珍,李世普.大鼠腹腔巨噬细胞的分离培养与鉴定[J].武汉理工大学学报,2009,31(9):41-42.
    [5]Mach F, Sehonbeek U, Sukllow GK, et al. Functional CD40 ligand is expressed on human vascular endothelial cells, smooth muscle cells, and macrophages. Implicationfor:CD4-CD40 ligand signaling in atherosclerosis.Proc Natl Acad Sci USA, 1997,94:1931-1936
    [6]Martin A, Foxall T, Blumberg JB, et al.Vitamin E inhibits Low-densitylipoprotein induced adhesion of monocytes to human aortic endothelial cell in Vitro. Arterioscler thtromb, 1997,17(2):429-436
    [7]Xenos ES, Stevens SL, Freeman MB, Cassada DC, Goldmna MH, Tennessee K. Nitric oxide mediates the effect of fluvastatin on intercellular adhesion molecule-1 and platelet endothelial cell adhesion molecule-1 expression on human endothelial cells. Annasl of Vascular Surgery,2005,19:1-7
    [8]Witkowska AM. Soluble ICAM-1:A market of vaseular in flammation and lifestyle. Cytokine,2005,31:127-134
    [9]MihoN, Ishida T, Kuwaba N, Ishida M, Shimote-AbeK, Tabuchi K. Role of the JNK Pathway in thrombin-induced ICAM-1 expression in endothelial cells. Cardiovascular Research, 2005,68 (2):289-295
    [10]Chiu JJ, Lee PL, ChenCN, LeeCl, ChangSF, ChenLJ, et al. Shear stress increases ICAM-1 and decreases VCAM-1 and E- selectin expressions induced by tumor necrosis factor-ain endothelial cells. Arteroscler Thromb Vasc Biol.2004,24:73-79
    [11]Williams KJ, Scalia R, Mazany KD et al. Rapid restoration of normal endothelial Functions in genetically hyperlipidemic mice by a synthetic mediator of reverse lipid transport. Arterioscler Thromb Vasc Biol 2000:20(4):1033-1039
    [12]Amberger A, Maczek C, Jurgens G, et al. Co-expression of ICAM-1, VCAM-1, ELAM-1 andHsp 60 in human arterial and venous endothelial cells in response to cytokines and oxidized low-density lipoproteins. Cell Stress Chaperones,1997, 2:94-103.
    [13]Dichtl W, Nilsson L, Goncalves I, et al. Very low-density lipoprotein activates nuclear factor-kappaB in endothelial cells. Circ Res,1999,84:1085-1094.
    [14]Cockerill GW, Rye KA, Gamble JR, et al. High density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules. Arterioscler Thromb Vasc Biol,1995,15:1987-1994.
    [15]刘永铭,严祥,张钲,等.他汀类调脂药物对高脂血症患者粘附的影响[J].中华心血管病杂志,2001,29(3):140-143
    [16]Hackman A, AbeY. Level of soluble cell adhesion molecules in patients with dyslipidemia[J]. Circulation,1996;93 (7):1334-1338
    [17]Scalia R, Appel J Z. Leukoeyte-endothelium interaction during the early stages of hypercholesterolemia in the rabbit: role of P-selectin, ICAM-1, and VCAM-1 [J]. Arterioscler Thromb Vasc Biol,1998:18 (7):1093-1100
    [18]Rollins BJ.Chemokines. Blood,1997,90:909-928
    [19]Muhaida N, Harada A, Matsushima K. Interleukin-8 (IL-8)and activating factor (MCAF/MCP-1) chemokines essentially involved in inflammatory and immune reaction. Cytokine Growth Factor Rev,1998,9:9-23
    [20]Cushing SD, Berliner JA, Valente AJ,et al. Minimally modified low density lipoprotein induces monocyte chemotactic protein 1 in human endothelial cells and smooth muscle cells.Proc Natl Acad Sci USA,1990,87:5134-5138
    [21]Yla-Herttuala S, Lipton B A, Rosenfeld ME, et al.Expression of monoeyte chemoattractant protein 1 in macrophagerich areas of human and rabbit atheroscleroticlesion. Proc Natl Acad Sci USA,1991,88:5252-5256.
    [22]王国平等.氧化修饰的低密度脂蛋白和极低密度脂蛋白对单核细胞MCP-1表达的影响[J].中华病理学杂志,1996,25(4):220-223
    [23]Virmani R,Kolodgie FD,Burke AP,et al. Lessons from sudden coronary death:a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vase Biol.2000; 20:1262-1275.
    [24]Hernandez-Presa MA, Bustos C, Ortego M, et al.ACE inhibitor quinapril reduces the arterial expression of NF-KB-dependent proinflammatory factors but not of collagen I in a rabbit model of atherosclerosis. Am J Pathol.1998; 153:1825-1837.
    [25]Chen YL,Chang,YJ,Jiang MJ. Monocyte chemotactic protein-1 gene and protein expression in atherogenesis of hypercholesterolemic rabbits. Atherosclerosis.1999; 143:115-123.
    [26]Fruebis J,Gonzalez V,Silvestre M,et al.Effect of probucol treatment on gene express ion of VCAM-1, MCP-1, and M-CSF in the aortic wall of LDL receptor-deficient rabbits during early atherogenesis. ArteriosclerThrombVasc iol.1997; 17:1289-1302.
    [27]Thompson RL, Summerbell CD, Hoper L, et al. Dietary advice givenby a dietitian versus other health professional of self-help resources to reduce blood cholesterol [J]. Coehrane Database Syst Rev,2003,3:1300-1366.
    [28]Cmiekshank AM, Oldroyde K, Cobbe S, et al. Serum IL-6 in Suspected myocardil infarction[J]. Lancet,1994,343(8904): 974-975.
    [29]成其讯,赵勇摘.IL-6在癌性恶病质中的作用可能是因其降低小鼠脂肪组织3T3-L;脂肪组织的脂蛋白醋酶活性[J].国外医学·免疫学分册,1993,5:284
    [30]Clafien PA, Camargo CA, JR, et al. Reasetant cytokines and neutrophil adhesion after warm ischemia in cirrhotic and noncirrhotic human livers [J]. Hepatology,1996,23:1456-1458
    [31]Cruickshank AM, Oldroyd KG, Cobbs.et al.Serum IL-6 in suspected myocardial infarction [J]. Lancet.1994; 343(8903): 974
    [32]Allan Ml, Rosario S, David J. Vaseular effeets of HMG-CoA reduetase inhibitors (statins)unrelated cholesterol lowering:new concepts for cardiovascular disease. Cardiovase Res,2001,49 (2):281-287.
    [33]Kothe H, Dalhoff K, Rupp J, et al.Hydroxylnethylglutaryl coenzylme A reduetase inhibitors modify the in flammatory response of human macrophages and endothelial cells infected with Chlamydia Pneumoniae. Circulation,2000, 101(15):1760-1763.
    [34]Ridker PM, Rifai N, StamPfer MJ, et al. Plasma coneentration of interleukin-6 and the risk of future myocardial infarction among apparently healthy men. Cireulation,2000, 101(15):1767-1772.
    [35]Eschwege E. The dysmetabolic syndrome, insulin resistance and increased cardiovascular (CV) morbidity and mortality in type2 diabetes:aetiological factors in the development of CV complications. Diabete Metab.2003Sep:29(4 pt2): 6519-6527.
    [36]陆再英,钟南山.内科学.北京:人民卫生出版社,2008:435-439
    [1]吕建敏,应华忠,徐孝平,等.高脂血症动物模型研究进展[J].浙江中医学院学报,2005,29(4):87-89.
    [2]王琼,乐薇,覃鹏飞,等.三种高脂血症实验性大鼠模型的比较[J].中国康复,2010,25(5):330-331.
    [3]孟晓萍,布艾加尔·哈斯木.动脉粥样硬化[M].北京:人民卫生出版社.2011:377-415
    [4]Scandinavian Simvastatin Survival Study Group:Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease:the Scandinavian Simvastatin Survival Study (4S). Lancet,1994; 344:1383-1389.
    [5]Shepherd J, Cobbe SM, Ford I,et al.For the West of Scotland Coronary Prevention Stuty Group:Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Eng J Med,1995; 333:1301-1307.
    [6]Glass CK,Witztum JL. Atherosclerosis. the roed ahead. Cell, 2001; 104:503-516.
    [1]许竹梅,赵水平.ATP结合盒转运子调节细胞内胆固醇流出及对动脉粥样硬化的影响[J].中国动脉硬化杂志,2002,10(5):449
    [2]罗丹.ATP结合框转运子A1的结构、功能及调控的研究进展[J];国外医学.临床生物化学与检验学分册;2003,(05):25
    [3]吕建敏,应华忠,徐孝平,等.高脂血症动物模型研究进展[J].浙江中医学院学报,2005,29(4):87-89.
    [4]王琼,乐薇,覃鹏飞,等.三种高脂血症实验性大鼠模型的比较[J].中国康复,2010,25(5):330-331.
    [5]Glomset JA. The plasma lecithin:cholesterol acyltransferase reaction. J Lipid Res.1968; 9:155-167
    [6]谢心.SR-BI表达调控在脂代谢相关性AS中的应用研究[J].中国医疗前沿,2007,3,1(3):49-50
    [7]Acton S, Rigotti A, Landschuiz K T, etal. Identification of scavenger receptor SR-BI as a high density lipoprotein receptor. Science,1996,271,518-520
    [8]Acton SL, Kozarsky KF, Rigotti A.The HDL receptor SR-BI: a new therapeutic target for atherosclerosis Molecular Medicine Today,1999,5:518-524
    [9]Vedhchalam C, Liu L, Nicket M, et al. Influence of apoA structureon the ABCAI-mediated efflux of cellular lipids[J].Biol Chem,2004,279 (48):49931-49939
    [10]Or am JF, Lawm RM. ABCA1:the gatekeeper for elim inating excess tissu echolesterol J lipid Res,2001,42:1173-1179.
    [11]唐朝克,代小艳,杨峻浩等.中国病理生理杂志,2006,22(7):1282-1288
    [12]唐朝克,易光辉,唐国华等.中国动脉硬化杂志,2003,11(4):304-305
    [13]曾芬,曾庆乐.PPAR α/γ双重激动剂的研究进展.海峡药学,2011,23(5):12
    [14]易光辉,唐朝克,莫中成等.PPAR在动脉粥样硬化发生与发展中的作用[J].生命的化学,2004,24(3):240-242
    [15]Lopez D, McLean MP. Activation of the rat scavenger receptor class B type 1 gene by PPARalpha [J]. Mol Cell Endocrinol, 2006,251 (1-2):67-77
    [16]秦永新,陈佰义.IGF-1及IGFBPs对成纤维细胞糖代谢及其功能的影响[J].国外医学呼吸系统分册,2005,25(5):337
    [17]朱艳霞,刘天庆等.IGF-1和动态微环境对脂肪干细胞向心肌细胞分化作用的研究[J].生物化学与生物物理进展,2009,36(12):1553
    [18]Qijin Xu, Shenghua L, i Yang Zhao, et a 1. Evidence that IGF binding protein-5 functions as a Ligand- independent transcriptional regulator in vascular smooth muscle cells [J]. Circ Res,2004,94 (5):46-54
    [1]赵水平.临床血脂学[M].长沙:湖南科学括术出版社,1997:169-198
    [2]血脂异常防治对策专题组.血脂异常防治建议.中华心血管病杂志,1997,25:169
    [1]初奎尘.高脂血症的中西医结合进展[J].中西医结合心脑血管病杂志,2003,1(6):350-351.
    [2]龚一萍.高脂血症的中医病因病机探讨[J].浙江中医学院学报,2000,24(2):23-24.
    [3]赵吉平,王燕平.针灸特定穴--理论与临床2版[M].北京:科学技术文献出版社,2005:110-111
    [4]解秸萍,李蔚,郭顺根,等.高脂血症大鼠肝细胞脂肪变性及脂蛋白代谢酶变化与电针丰隆穴的干预效应[J].中国组织工程研究与临床康复,2007,11(43):81-87
    [5]解秸萍,李蔚,农艳,等.丰隆穴对高脂血症大鼠不同脏器SOD、 MDA的影响[J].中国针灸,2008,28(4):29-30
    [6]张红星,万文俊,周利,等.电针丰隆穴对高脂血症大鼠血脂及CGRP的影响[J].中国康复,2007,22(2):81-83
    [7]张唐法,万文俊,张红星.电针丰隆穴治疗高脂血症的多中心观察[J].中国临床康复,2006,10(19);17-19.
    [1]方永奇.痰证的血液循环特征初探[J].湖北中医杂志,1992(6):33-35
    [2]肖洪彬,王峻,刘丽萍,等.补阳还五汤对老龄大鼠血液流变学的影响研究[J].中药药理与临床,2007,23(5):21-24
    [3]胡晓灵,周伟峰.复方降脂散治疗原发性高脂血症临床研究[J].新疆中医药,2001,19(3):19-20
    [4]陈孝东,曹勇军,王引明,等.参芎注射液对脑缺血再灌注大鼠行为学和血液流变学的影响[J].中国血液流变学杂志,2006,16(1):43-45
    [1]兰青,尹美珍,李世普.大鼠腹腔巨噬细胞的分离培养与鉴定[J].武汉理工大学学报,2009,31(9):41-42.
    [2]Elangbam CS, TylerRD. Lightfot RM. Peroxisme proliferators-aetivated receptors in atheroselerosis and inflammation; an update[J]. Toxicol Pathol,2001,29; 224.231
    [3]于燕,刘继兰,王菊英,等.土鳖虫水提液对实验性高脂血症大鼠血管内皮细胞的保护作用.山东大学学报(医学版).2002,40(5):398-400.
    [4]StollG, BendszusM. Inflammation and atherosclerosis:novel insights into plaque formation and destabilization [J]. Stroke,2006,37(7):1923-932.
    [5]5 Westendorf T, Graessler J, Kopprasch S. HyPoehlorite-oxidized low-density Lipoprotein upregulates CD36 and PPARγ mRNA expression and modulates SR-BI gene expression in murine maerophages. Mol Cell Bioehem,2005 277:143-152.
    [6]Feingold K R, Hardardottir I, Grunfeld C. Beneficial effeets of cytokine indueed hyperlipidemia [J]. Z Ernahrungswiss, 1998,37 Suppl:66-74.
    [7]Ruan X Z, Varghese Z, Powis S H, et al. Dysregulation of LDL receptor under the influence of inflammatory cytokines:a new pathway for foam cell formation[J]. Kidney Int,2001, 60(5):1716-1725.
    [8]Khovidhunkit W, Kim M S, Memon R A, et al. Effects of infection and inflammation on lipid and lipoprotein metabolism:mechanisms and consequences to the host [J].J Lipid Res,2004,45 (7):1169-1196.
    [9]Ohashi R, Mu H, Wang X, et al. Reverse cholesterol transport and cholesterol efflux in atherosclerosis [J].QJM,2005, 98(12):845-856.
    [10]Kwon HM, Choi YJ, Jeong YJ, KangSW, Kang IK, LimSS, et al. Anti-inflammatory inhibition of endothelial cell adhesion molecule expression by flavone Derivatives. J Agric Food Chem,2005,53:5150-5157
    [11]林秋伟.细胞间黏附分子-1与心血管疾病关系研究进展[J].岭南心血管杂志,2006,12(2):146-148
    [12]贾卫国,安振海.可溶性黏附因子-1[J].华西医学,1997,12(4):465-466
    [13]Witkowska AM. Soluble ICAM-1:A market of vaseular in flammation and lifestyle. Cytokine,2005,31:127-134
    [14]MihoN, Ishida T, Kuwaba N, Ishida M, Shimote-AbeK, Tabuchi K. Role of the JNK Pathway in thrombin-induced ICAM-1 expression in endothelial cells.Cardiovascular Research, 2005,68(2):289-295
    [15]Gorgoulis VG, Zacharatos P, Kotsinas A, Kletsas D, Mariatos G, Zoumpourlis V, et al. P53 activates ICAM-(CD54) expression in an NF-kB independent manner. EMBO J,2003,22:1567-1578
    [16]Mach F, Sehonbeek U, Sukllow GK, et al. Functional CD401 igand is expressed on human vascular endothelial cells, smooth muscle cells, and macrophages. Implicationfor:CD4-CD40 ligand signaling in atherosclerosis. Proc Natl Acad Sci USA, 1997,94:1931-1936
    [17]Martin A, Foxall T, Blumberg JB, et al.Vitamin E inhibits Low-densitylipoprotein induced adhesion of monocytes to human aortic endothelial cell in Vitro. Arterioscler thtromb,1997,17 (2):429-436
    [18]Xenos ES, Stevens SL, Freeman MB, Cassada DC, Goldmna MH, Tennessee K. Nitric oxide mediates the effect of fluvastatin on intercellular adhesion molecule-1 and platelet endothelial cell adhesion molecule-1 expression on human endothelial cells. Annasl of Vascular Surgery,2005,19:1-7
    [19]Witkowska AM. Soluble ICAM-1:A market of vaseular in flammation and lifestyle. Cytokine,2005,31:127-134
    [20]MihoN, Ishida T, Kuwaba N, Ishida M, Shimote-AbeK, Tabuchi K. Role of the JNK Pathway in thrombin-induced ICAM-1 expression in endothelial cells.Cardiovascular Research, 2005,68(2):289-295
    [21]Chiu JJ, Lee PL, ChenCN, LeeCl, ChangSF, ChenLJ, et al. Shear stress increases ICAM-1 and decreases VCAM-1 and E-selectin expressions induced by tumor necrosis factor-ain endothelial cells. Arteroscler Thromb Vasc Biol.2004,24:73 79
    [22]Williams KJ, Scalia R, Mazany KD et al. Rapid restoration of normal endothelialFunctions in genetically hyperlipidemic mice by a synthetic mediator of reverse lipid transport.Arterioscler Thromb Vasc Biol 2000:20 (4):1033-9
    [23]张露芬,程金莲,严洁.电针心经腑穴对大鼠高血脂症血浆内皮素、降钙素基因相关肤影响的实验观察.中国中医基础医学杂志.2001,7(5):60-62
    [24]Amberger A, Maczek C, Jurgens G, et al. Co-expression of ICAM-1, VCAM-1, ELAM-1 andHsp 60 in human arterial and venous endothelial cells in response to cytokines and oxidized low-density lipoproteins. Cell Stress Chaperones,1997, 2:94-103.
    [25]Dichtl W, Nilsson L, Goncalves I, et al. Very low-density lipoprotein activates nuclear factor-kappaB in endothelial cells. Circ Res,1999,84:1085-1094.
    [26]Cockerill GW, Rye KA, Gamble JR, et al. High density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules. Arterioscler Thromb Vasc Biol,1995,15:1987-1994.
    [27]刘永铭,严祥,张钲,等.他汀类调脂药物对高脂血症患者黏附分子的影响[J].中华心血管病杂志,2001,29(3):140-143
    [28]Hackman A, Abe Y. Level of soluble cell adhesion molecules in patients with dyslipidemia[J]. Circulation, 1996; 93 (7):1334-1338
    [29]Scalia R, Appel J Z. Leukoeyte-endothelium interaction during the early stages of hypercholesterolemia in the rabbit:role of P-selectin, ICAM-1, and VCAM-1[J]. Arterioscler Thromb Vase Biol,1998:18 (7):1093-1100
    [30]Yla-Herttuala S, Lipton BA, Rosenfeld ME, et al. Expression of monocyte chemoattractant protein 1 in macrophage-rich areas of human and rabbit atherosclerotic lesions. Proc Natl Acad Sci USA,1991,88(12):5252-5256.
    [31]Rollins BJ.Chemokines.Blood,1997,90:909-928
    [32]Muhaida N, Harada A, Matsushima K. Interleukin-8(IL-8)and activating factor (MCAF/MCP-1) chemokines essentially involved in inflammatory and immune reaction. Cytokine Growth Factor Rev,1998,9:9-23
    [33]Cushing SD,Berliner JA,Valente AJ, et al.Minimally modified low density lipoprotein induces monocyte chemotactic protein 1 in human endothelial cells and smooth muscle cells.Proc Natl Acad Sci USA,1990,87:5134-5138
    [34]Yla-Herttuala S, Lipton B A, Rosenfeld ME, et al. Expression of monoeyte chemoattractant protein 1 in macrophagerich areas of human and rabbit atheroscleroticlesion. Proc Natl Acad Sci USA,1991,88:5252-5256.
    [35]王国平等.氧化修饰的低密度脂蛋白和极低密度脂蛋白对单核细胞MCP-1表达的影响[J].中华病理学杂志,1996,25(4):220-223
    [36]Virmani R, Kolodgie FD,Burke AP, et al. Lessons from sudden coronary death:a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vase Biol.2000; 20:1262-1275.
    [37]Hernandez-Presa MA,Bustos C,Ortego M, et al.ACE inhibitor quinapril reduces the arterial expression of NF-KB-dependent proinf lammatory factors but not of collagen I in a rabbit model of atherosclerosis.Am J Pathol.1998; 153:1825-1837.
    [38]Chen YL, Chang YJ,Jiang MJ.Monocyte chemotactic protein-1 gene and protein expression in atherogenesis of hypercholesterolemic rabbits. Atherosclerosis.1999; 143:115-123.
    [39]Fruebis J, Gonzalez V, Silvestre M, et al. Effect of probucol treatment on gene expression of VCAM-1,MCP-1,and M-CSF in the aortic wall of LDL receptor-deficient rabbits during early atherogenesis. Arterioscler Thromb Vase Biol.1997; 17:1289-1302.
    [40]Yin K et al. ABCA1:a possible link between inflammation and reverse cholesterol transport. Mol Med,2010,16:438-449
    [41]汤石林,唐朝可.急性应答与胆固醇逆向转运[J].生命的化学,2011,31(3):438-441
    [42]Thompson RL, Summerbell CD, Hoper L, et al. Dietary advice givenby a dietitian versus other health professional of self-help resources to reduce blood cholesterol [J]. Coehrane Database Syst Rev,2003,3:1300-1366.
    [43]RuanH, HacohenN, Golub TR, et al. Tumor necrosis factor-alpha suppresses adipocyte-specific genes and activates expression of preadipocyte genes in3T3-L1 adipocytes: nucleac factor-kappaB actb at ion by TNF-α is obligatory[J]. Diabetes.2002; 51(5):1319.
    [44]CmiekshankAM, Oldroyde K, Cobbe S, et al. Serum IL-6 in Suspected myocardil infarction [J]. Lancet,1994,343(8904): 974-975.
    [45]成其讯,赵勇摘.IL-6在癌性恶病质中的作用可能是因其降低小鼠脂肪组织3T3-L;脂肪组织的脂蛋白醋酶活性[J].国外医学·免疫学分册,1993,5:284
    [46]Clafien PA, Camargo CA, JR, et al. Reasetant cytokines and neutrophil adhesion after warm ischemia in cirrhotic and noncirrhotic human livers [J]. Hepatology,1996,23:1456
    [47]Schieffer B, Schieffer E, Hilfiker D et al. Expression of arrgiot ens in II and interleukin 6 in human coronary atherosclerotic plaques:potential implications for inflammat ion and plaque instability [J]. Circulation,2000; 101 (12):1372-1378
    [48]Huber S A, Sakkinen P, Conze D et al.Interleukin-6 exacerbates early atherosclerosis in mice [J]. Arter ioscler Thromb Vasc Biol,1999; 19(10):2364-2367
    [49]Cruickshank AM, Oldroyd KG, Cobbs.et al. Serum IL-6 in suspected myocardial infarction [J]. Lancet.1994; 343(8903): 974
    [50]Choussat R, Montalescot G, Collet JP, et al. Effeet of prior exposure to Chlamydia pneumonias, or cytomegalovirus on the degree of inflammation and oneyear prognosis of patients with unstable angina pectoris or non-Q ware myocardial infarction[J]. A M J Cardiol.2000:86 (4):379-384.
    [51]Allan Ml, Rosario S, David Jl. Vaseular effeets of HMG-CoA reduetase inhibitors(statins)unrelated cholesterol lowering:new concepts for cardiovascular disease. Cardiovase Res,2001,49 (2):281-287.
    [52]Kothe H, Dalhoff K, Rupp J, et al. Hydroxylnethylglutaryl coenzylme A reduetase inhibitors modify the in flammatory response of human macrophages and endothelial cells infected with Chlamydia Pneumoniae. Circulation,2000, 101 (15):1760-1763.
    [53]Ridker PM, Rifai N, StamPfer MJ, et al. Plasma concentration of interleukin-6 and the risk of future myocardial infarction among apparently healthy men. Circulation,2000, 101(15):1767-1772.
    [54]Ikejima K, Honda H, Yoshikawa M, et al.Leptin augments inflammatory and prof ibrogenic responses in the murine liver inducedby hepatotoxic chemicals[J]. Hepatology,2001,34 (2):288-297.
    [1]廖端芳,唐朝克.胆固醇逆向转运基础与临床[M].北京:科学出版社.2009:25-26
    [2]许竹梅,赵水平.ATP结合盒转运子调节细胞内胆固醇流出及对动脉粥样硬化的影响[J].中国动脉硬化杂志,2002,10(5):449
    [3]Glomset JA. The plasma lecithin:cholesterol acyltransferase reaction. J Lipid Res.1968; 9:155-167
    [4]Acton SL, Kozarsky KF, Rigotti A. The HDL receptor SR-BI: a new therapeutic target for atherosclerosis Molecular Medicine Today,1999,5:518-524
    [5]Vedhchalam C, Liu L, Nicket M, et al. Influence of apoA structureon the ABCAI-mediated efflux of cellular lipids[J].Biol Chem,2004,279 (48):49931-49939
    [6]Schmilz G, Langman T. Structure, function and regulation of the ABCA1 gene product [J]. Curr opin lipidol,2001,12 (2):129-140.
    [7]Marcil M, Brook-Wilson A, Clee SM, et al.Mutaion in the ABClgene in familiarHDL deficiencywith defective cholesterol efflux. Lancet,1999,354:1341-346
    [8]Higgins CF.Flip-flog:the transmembrane translocation of lipids.Cell,1994,79:393-395
    [9]Francis GA, KaoppRH, OramJF. Defective removal of cellular cholesterol and phospholipids by apolipoprotein A-l in Trangier disease. J Clin Invest,1995,96:78-87
    [10].Santamarina-Fojo S, Peterson K, Knapper C, et al.Complete genomic sequence of human ABCAlgene:Analysis of human and mouse ATP-binding cassette A promoter.ProcNatlAcadSci USA, 2000,97:7 987-992
    [11]罗丹.ATP结合框转运子A1的结构、功能及调控的研究进展[J];国外医学.临床生物化学与检验学分册;2003,(05):25
    [12]Langmann T et al. Biochem Biophys Res Commun,1999,257 (1):29-33
    [13]唐朝克,代小艳,杨峻浩等.中国病理生理杂志,2006,22(7):1282-1288
    [14]唐朝克,易光辉,唐国华等.中国动脉硬化杂志,2003,11(4):304-305
    [15]唐朝克,杨永宗.三磷酸腺苷结合盒转运体A1在转基因小鼠中的作用[J].中国老年学杂志,2005,25(2):225-227.
    [16]唐朝克,严鹏科,杨永宗.三磷酸腺苷结合盒转运体A1在巨噬细胞胆固醇流出中的作用[J].中国病理生理杂志,2003,19(10):1427-1431.
    [17]唐朝克,杨永宗.LXR和ABCA1对体内胆固醇代谢的调节作用[J].生命的化学,2003,(05):23
    [18]Tsai JY, Su KH, Shyue SK, et al. EGb761 ameliorates the formation of foam cells by regulating the expression of SR-A and ABCA1:role of haem oxygenase-1 [J]. CardiovascRes, 2010,88(3):415-423.
    [19]Le Goff W, Peng DQ, Settle M, et al. Cyclosporin A traps ABCA1 at the plasma membrane and inhibits ABCA1-mediated lipid efflux to apolipoprotein A-I [J]. Arterioscler Thromb Vasc Biol,2004,24(11):2155-2161.
    [20]Vedhchalam C, Liu L, NicketM, et al. Influence of apoA structure on the ABCAl-mediated efflux of cellular lipids [J]. Biol Chem,2004,279 (48):49931-49939.
    [21]Oram JF, Lawm RM. ABCA1:the gatekeeper for elim inating excess tissu echolesterol J lipid Res,2001,42:1173-1179.
    [22]Soro-Paavonen A, Nauk karinen J, Lee-RueckertM, et al. Common ABCA1 variants, HDL. J Lipid Res,2007,48:1409-1416.
    [23]Repa JJ, Turley SD, Lobaccaro JA, et al. Regulation of absorption and ABCAl-mediated efflux of cholesterol by RXR heterod imers science,2000,289:1524-1529.
    [24]张晓菲,谭晓华,杨磊.ABCA1在胆固醇逆转运中作用的研究进展[J].健康研究,2010,(30):3
    [25]Vedhchalam C, Liu L, Nicket M, et al. Influence of apoA structureon the ABCA1-mediated efflux of cellular lipids [J].Biol Chem,2004,279 (48):49931-49939
    [26]赵国军,唐朝克.?apoA-1与ABCA1结合激活信号通路并介导细胞内胆固醇流出[J].中南医学科学杂志,2011,39(4)
    [27]Remaley AT, Stonik JA, Demosky SJ, et al. Apolipoprotein specificity for lipid efflux by the human ABCAI transporter.Biochem Biophys Res Commun,2001,280 (3): 818-823
    [28]Dhaliwal B S, Steinbrecher U P. Scavenger receptors and oxidized low density lipoproteins [J]. Clin Chim Acta,1999, 286 (1-2):191-205.
    [29]Jane E M, Philip R T, Shervanthi H V, et al. Biochemistry and cell biology of mammalian scavenger receptors [J] Atherosclerosis,2005,182 (1):1-15.
    [30]巫晔翔,洪斌,司书毅.高密度脂蛋白受体(SR-BI)和胆固醇逆转运[J].中国生物工程杂志,2003,23(5):21-23
    [31]Krieger M, Kozarsky K. Influence of the HDL receptor SR-B I on atheroselerosis.Curr Opin Lipidol,1999,10:491-497
    [32]Acton S, Rigotti A, Landschulz K T, et al. Identification of scavenger receptor SR-BI as a high density lipoprotein receptor. Science,1996,271,518-520
    [33]Trigatti B L, RigottiA, BraunA. Cellularand physiol-ogical roles of SR-BI, a lipoproteinrecept or which medial s selective lipid uptake. Biechim Biophys Acta,2000,15,29 (1-3):276-286
    [34]张青海,易光辉,李媛彬等.B类1型清道夫受体表达调控与信号转导通路.中国生物化学与分子生物学报.2009,25(11):1003-1009
    [35]Thomas J, F Nileland, Jared T, et al. cholesterol-elevating drugs on the in vitro activity.
    [36]Ken-ichi Hirano, Chiaki Ikegami, Ken-ichi T. Enhances the Expression of Human Hepatic Scaveng Type Ⅰ, Possibly Through a Species-Specific Me Thromb. Vasc. Biol,2005; 25:2422-2427
    [37]Acton SL, Kozarsky KF, Rigotti A. The HDL receptor SR-BI: a new therapeutic target for atherosclerosis Molecular Medicine Today,1999,5:518-524.
    [38]Cao WM, Murao K, Imachi H, etal. Insulin-like growth factor-I regulation of hepatic scavenger receptor class BI[J]. Endocrinology,2004,145(12):5540-5547
    [39]Fowler DJ, Nicolaides KH, Miell JP. Insulin-like growth factor binding protein-1 (IGFBP-1):a muhifunctional role in the human female reprodu-ctive tract [J]. Hum Reprod Date, 2000,6(5):495-504.
    [40]Li XA, Titlow WB, Jacks on BA, etal. High density lipoprotein binding to scavenger receptor, class B, type I activates endothelial nitric-oxide synthase in a ceramide-dependent manner [J]. J Biol Chem,2002,277(13):11058-11063
    [41]Assanasen C, Mineo C, Seetharam D, et al. Cholesterol binding, efflux, and a PDZ-interact ing domain of scavenger receptor-BI mediate HDL-initiated signaling [J]. J Clin Invest,2005,115 (4):969-977
    [42]Zhu W, Saddar S, Seetharam D, et al. The scavenger receptor classB type I adaptor protein PDZK 1 maintains endothelial monolayer integrity[J]. Circ Res,2008 102(4):480-487
    [43]Zhang Y, Ahmed AM, Me Farlane N, et al. Regulating of SR-BI-mediated selective lipid uptake in Chinese hamster ovary-derived cells by protein kinese signaling pathways.J Lipid Res,2007; 48 (2):405-416
    [44]Grewal T, de Diego I, Kirchhoff MF, et al. High density lipoprotein induced signaling of the MAPK pathway inv olves scavenger receptor type BI-mediated activation of Ras [J]. J Biol Chem,2003,278(19):16478-16481
    [45]Rentero C, Evans R, Wood P, et al. Inhibition of H-Ras and MAPK is compensated by PKC-dependent pathways in annexin A6 expressing cells [J]. Cell Signal,2006,18 (7): 1006-1016
    [46]Zhang Y, Ahmed AM, McFarlane N, et al. Regulation of SR-BI-mediated selective lipid uptake in Chinese hamster ovary -derived cells by protein kinase signaling pathways [J]. J Lipid Res,2007,48(2):405-416
    [47]Krause BR, Auerbach BJ. Reverse cholesterol transport and future pharmacological approaches to the treatment of atherosclerosisl Curr Opin Investig Drugs,2001,2: 37523811
    [48]曾芬,曾庆乐.PPAR α/γ双重激动剂的研究进展.海峡药学,2011,23(5):12
    [49]易光辉,唐朝克,莫中成等.PPAR在动脉粥样硬化发生与发展中的作用[J].生命的化学,2004,24(3):240-242
    [50]Ma lerod L, SporstolM, Juvet LK, et al. Hepatic scavenger receptor class B, type Ⅰ is stimulated by peroxisome prolifera to ractivated receptor gamma and hepatocyte nuclear factor 4alpha [J]. Biochem Biophys ResCommun,2003, 305 (3):557-565
    [51]尹小波,莫中成,石金凤等.丙丁酚对高脂高胆固醇饮食小鼠肝脏SR-BI表达的影响[J].南华大学学报,2010,38(5):6-10
    [52]Cao WM, Murao K, Imachi H, etal. Insulin2like growth factor2I regulation of hepatic scavenger receptor class BI [J]. Endocrinology,2004,145 (12):5540-5547
    [53]李丽平等.肝病患者血清胰岛素样生长因子-1测定的临床意义[J].山东医药,2006,46(10):65
    [54]武海亮,刘雅娟,刘芳,等.代谢综合征患者胰岛素样生长因子-1及胰岛素抵抗与内皮损害的关系[J].宁夏医学杂志.2011,33(2):99-101
    [55]朱艳霞,刘天庆等.IGF-1和动态微环境对脂肪干细胞向心肌细胞分化作用的研究[J].生物化学与生物物理进展,2009,36(12):1553
    [56]秦永新,陈佰义.IGF-1及IGFBPs对成纤维细胞糖代谢及其功能的影响[J].国外医学呼吸系统分册,2005,25(5):337
    [57]Colao A, Spiezia S, Di Somma C, et al.Circulat ng insulin like growth factor-1 levels are correlated with the atherosclerotic prof ilein healthy subjects independently of age [J]. J Endocrinol Invest,2005,28(5):440-448
    [58]Qijin Xu, Shenghua L, i Yang Zhao, et al. Evidence that IGF binding protein-5 functions as a Ligand- independent transcriptional regulator in vascular smooth muscle cells [J]. Circ Res,2004,94 (5):46-54
    [1]王晓宁.针刺治疗高脂血症的临床观察[J].针灸临床杂志,2005,21(9);9-10.
    [2]黄钰玲.针刺治疗痰浊阻遏型高脂血症的临床研究[J].四川中医,2008,26(6):113-114
    [3]肖伟,李飞.针药并用对高脂血症患者血脂及C反应蛋白的影响[J].中医药临床杂志,2009,21(7):14-15.
    [4]隋永杰,张桂侠,张勇等.三阴交穴为主针刺治疗脾虚湿阻型单纯性肥胖及对血脂的影响[J].陕西中医,2010,31(2):213-214
    [5]蔡辉,袁爱红.针刺对高脂血症大鼠血脂及血清一氧化氮含量和髓过氧化物酶活力的影响[J].河北中医,2010,9,32(9):1404
    [6]王永玲,郭勇,千新来,等.针刺肥胖合并高脂血症大鼠时瘦素基因对肝细胞凋亡的影响[J].实用医学杂志,2010,26(10):1723
    [7]张红星,黄国付,张唐法等.电针丰隆穴治疗高脂血症的临床疗效[J].中国康复2006,21(6):372-373.
    [8]朱雅萍.电针治疗高脂血症60例[J].吉林中医药,2001;(4):43-45
    [9]张唐法,万文俊,张红星.电针丰隆穴治疗高脂血症的多中心观察[J].中国临床康复,2006,10(19):17-18.
    [10]胡幼平,卢松,青林波等.电针丰隆、阴陵泉治疗原发性高脂血症临床疗效研究[J].针灸临床杂志,2008,24(3):6-7.
    [11]周利,万文俊.电针“丰隆”穴对高脂血症大鼠NO、ET及CGRP的影响[J].中国针灸,2008,28(1):57-60.
    [12]杨金梅,张唐法,张红星,等.电针丰隆穴早期干预金黄地鼠高脂血症的机制[J].中国康复,2011,26(1):89-90.
    [13]张红星,万文俊,周利,等.电针丰隆穴对高脂血症大鼠血脂及CGRP的影响[J].中国康复,2007,22(2):81-83
    [14]齐凤军,孙国杰.电针干预高脂血症大鼠动脉粥样硬化形成的实验研究[J].上海针灸杂志,2007,26(6):41-43.
    [15]唐胜修,唐萍.丰隆、足三里穴位注射治疗高脂血症的临床研究[J].广西医学,2000,22(6);1402-1404.
    [16]刘运珠,岁继红,宁发锦,等.穴位注射对高脂血症患者血脂的影响[J].上海针灸杂志,2007;26(2):15-16.
    [17]毛红蓉,徐浩.复方当归注射液注射丰隆穴治疗高脂血症的临床研究[J].湖北中医杂志,2007,29(10):15-16
    [18]何玲,郑云,任磊,等.穴位注射对糖尿病大鼠高脂血症血清N0、SOD影响的实验研究[J].中华中医药学刊,2009,27(10):21-22
    [19]蒋湘莲,李梓民,李东阳,等.穴位注射复方丹参液对高脂血症大鼠疗效观察[J].南华大学学报医学版,2006,34(1):34-35
    [20]栗茂.针药结合治疗老年高脂血症46例[J].云南中医中药杂志,2008,29(1):28-30
    [21]肖伟,李飞.针药并用对高脂血症患者及c反应蛋白的影响[J].中医药临床杂志,2009,2,21(1):14-15
    [22]马奎军.中药配合针刺丰隆穴治疗高脂血症[J].中国中医药现代远程教育,2008,5,6(05):46-47
    [23]巫祖强,刘吉昌,栗漩.针刺配合灯盏细辛治疗颈动脉斑块的临床研究[J].光明中医,2008,3,23(3):300-302
    [24]常延平,张富亮,张其梅.活血降浊汤配合针刺治疗高脂血症疗效观察[J].实用中医内科杂志,2008,22(12):56-58
    [25]杨骏,李飞,张庆萍等.针药结合对高血压复合高脂血症大鼠血管内皮细胞的影响[J].中国针灸,2006,26(12):575-575.
    [26]高耀华,王竹行,陈新黔,等.降脂药灸治疗中老年高脂血症的临床研究[J].中国针灸,2000,(2);77-79
    [27]魏红沁,丁春华,张晴,等.艾灸治疗高脂血症临床观察[J].上海针灸杂志,2009,12,28(12):698-699
    [28]王国明,沈玲哲,温峰云,等.瘢痕灸治疗高脂血症40例临床观察[J].中国中医药信息杂志,2000,7(11):72-73.
    [29]牛晓红,金红,宋剑南,等.灸神阙穴降脂抗氧化作用的研究[J]中国中医基础医学杂志,2003,9(10):71-77.
    [30]严洁,常小荣,岳增辉等.隔药饼灸对高脂血症兔血脂含量的影响[J].中国中医药科技,2004,11(6):358-360.
    [31]岳增辉,常小荣,严洁,等.隔药饼灸对兔高脂血症合并动脉粥样硬化主动脉血管细胞黏附分子-1 mRNA表达的影响[J].针刺研究,2006,31(3):145-148.
    [32]王倩,丛萃,等.穴位埋线治疗肥胖型高脂血症52例疗效观察[J].新中医,2005;37(6):64-65.
    [33]李艳芬,庄礼兴,朱晓平.穴位埋线治疗高脂血症的临床研究[J].辽宁中医杂志2011;31(6):32-35
    [34]丛莘,金庆文,李莉芳,等.穴位埋线治疗肥胖型高脂血症及对血脂水平的影响[J].中国社区医师,2006,22(315):45-47
    [35]毛红蓉,王凌云,张红星,等.比较穴位埋线与药物治疗高脂血症的作用[J].中国康复,2009,8,24(4):25-27
    [36]袁俏梅.穴位埋线对实验性高脂大鼠的影响[J].上海针灸杂志,2003,(9):26-28
    [37]李巍,谭洛,于波等.氦-氖激光穴位针刺治疗高脂血症临床研究[J].针灸临床杂志,2008,24(8):3-5.
    [38]张丽,李东书,盛丽.磁针治疗单纯性肥胖症并发高脂血症的疗效观察[J].上海针灸杂志,2003,22(2);7-9
    [39]乔淑章,陈莉,康文巧,等.半导体激光穴位照射治疗高脂血症60例[J].河北中医,2005,27(3);208-209
    [40]韩丽英.穴位贴敷治疗高脂血症临床观察[J].辽宁中医杂志,2003;30(6):46-48
    [41]李琳,汪振宇.体穴与耳穴治疗青少年单纯性肥胖症及对血脂代谢的影响[J].中国针灸,2006,26(3);173-177.

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