动脉粥样硬化兔纤溶酶原激活物抑制物-1的表达及与血脂相关性的研究

目的:探讨动脉粥样硬化(AS)兔血清和粥样硬化斑块中纤溶酶原激活物抑制物-1(PAI-1)的表达以及与血脂的相关性。方法:雄性大耳白兔随机分成正常饮食组和高脂饮食组,每组8只,饲养16周。2组动物均于饲养0、8、16周采耳缘静脉血,检测血清中胆固醇(TC)、低密度脂蛋白(LDL)以及PAI-1的水平;16周后处死动物,应用免疫组化方法检测PAI-1在主AS斑块中的表达。结果:正常饮食组0、8、16周血清中TC、LDL和PAI-1水平差异无统计学意义(均P>0·05);高脂饮食组8周后血清中TC、LDL和PAI-1水平较0周显著增加(均P<0·01),16周较8周增加更为明显(均P<0·01);免疫组化结果显示高脂饮食组主动脉壁PAI-1的表达明显高于对照组(P<0·01)。结论:AS的发生伴有血清和粥样斑块中PAI-1表达增加,表达量与血清TC、LDL呈正相关。     

黄芩茎叶总黄酮对高脂血症兔主动脉VCAM-1、ICAM-1表达的影响

目的观察黄芩茎叶总黄酮(SSTF)对高脂血症兔主动脉血管细胞黏附分子(VCAM)-1、细胞间黏附分子(ICAM)-1表达的影响,探讨SSTF抗动脉粥样硬化(AS)的可能机制。方法 24只健康雄性家兔随机分为正常对照组(6只),喂养普通饲料,动脉粥样硬化模型组(18只),喂养高脂饲料。8w后,将AS模型组再随机分为模型组,继续喂养高脂饲料,SSTF治疗组,喂养高脂饲料并灌胃给予SSTF(100、200mg·kg-1.d-1),治疗4w后,处死家兔,测定各组家兔TC、TG、LDL-C,取主动脉做病理切片,免疫组化检测主动脉VCAM-1、ICAM-1的表达。结果 SSTF可以降低高脂饮食兔血清TC、TG、LDL-C水平,作用效果呈剂量依赖性。SSTF能够逆转动脉粥样程度、抑制VCAM-1、ICAM-1的表达。结论 SSTF具有抗AS作用,可能与通过下调VCAM-1、ICAM-1表达,从而抑制血管壁炎症反应有关。     

冠心康对高脂血症兔血管LOX-1表达的影响

目的观察冠心康对高脂血症兔主动脉血凝素样氧化低密度脂蛋白受体1（lectin—like low density lipoprotein receptor-1，LOX1）表达的影-响。方法24只兔随机分三组：空白组，模型组，冠心康干预组，喂食高脂饲料方法建立兔高脂血症模型。分别于0周、8周时耳中央动脉采血检测血清总胆固醇（TC）、低密度脂蛋白胆固醇（LDL—C）水平。8周时处死动物，RT—PCR法检测兔主动脉LOX-1 mRNA表达，免疫组化法检测主动脉LOX-1蛋白表达。结果高脂组血管LOX-1表达显著增加，与之对比，冠心康明显下调了血管LOX-1的表达水平（P〈0．05）。结论冠心康的抗动脉粥样硬化（Atheroscierosis，AS）作用，部分是通过下调LOX-1表达实现的。     

阿托伐他汀抗动脉粥样硬化的机制

目的通过观察阿托伐他汀对家兔主动脉粥样硬化消退作用和对血管细胞黏附分子-1(VCAM-1)和纤溶酶原激活物抑制物-1(PAI-1)的影响,探讨其抗动脉粥样硬化(AS)的可能机制.方法24只大耳白兔随机分为常规饲料组、胆固醇饲料组和阿托伐他汀组,饲养16周.观察实验前后血清胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)、VCAM-1、PAI-1水平和体重的变化,处死动物后取主动脉进行病理学检查,采用免疫组化方法测定主动脉粥样硬化局部VCAM-1和PAI-1阳性表达百分数.结果实验前3组动物血清TC、TG、LDL、VCAM-1和PAI-1水平无显著差异(P＞0.05),16周后与胆固醇饲喂组比较,阿托伐他汀明显降低血清TC、LDL、VCAM-1和PAI-1水平,明显减少斑块/内膜面积比(0.161±0.027比0.281±0.037,P＜0.01);明显减少内膜厚度(38.11±6.02比67.47±7.13)μm;明显减少内膜/中膜比(0.391±0.213比0.878±0.370,P＜0.01).阿托伐他汀明显减少VCAM-1和PAI-1的阳性表达(P＜0.01).结论AS的发生伴有VCAM-1和PAI-1的过度表达,阿托伐他汀通过抑制它们的表达减轻AS病变可能是其抗AS机制之一.     

咪达普利在兔动脉粥样硬化干预中的作用及机制

将30只纯种大白兔随机分为三组各10只.A组以普通饲料喂养;B组采用高脂饮食(饲料中含1%胆固醇及5%猪油)喂养;C组以高脂饮食喂养并灌服咪达普利3 mg/(kg·d).8周后测定各组血清总胆固醇(TC)、甘油三酯(TG)及低密度脂蛋白胆固醇(LDL-C)水平,免疫组化法观察动脉细胞黏附分子-1(VCAM-1)的表达情况.结果B.C组血清TC、TG、LDL-C水平表达无显著差异,但均显著高于A组(P均＜0.01);C组内膜增生及VCAM-1水平明显低于B组.认为咪达普利可明显抑制AS的发生;其机制可能为降低AS血管VCAM-1表达,抑制AS过程中的炎性反应.     

高脂饮食诱导胰岛素抵抗大鼠血清Apelin与VCAM-1的关系

目的研究高脂饮食诱导的胰岛素抵抗大鼠血清Apelin与血清血管细胞间黏附分子-1（VCAM-1）的水平,探讨Apelin与VCAM-1、高胰岛素血症、肥胖及糖脂代谢等的相关性。方法 W istar雄性大鼠30只,随机平均分为正常对照组和高脂饮食组。行高胰岛素—正葡萄糖钳夹试验确认胰岛素抵抗大鼠造模成功后,测定血清Ape-lin-36、VCAM-1、空腹血清胰岛素（FINS）、空腹血糖（FBG）、TG、TC等指标。结果高脂饮食组血清中Apelin-36、VCAM-1均高于正常对照组（P〈0.01）。相关分析显示血清Apelin与VCAM-1、FINS、腹内脂肪含量、FBG、TG、TC、体质量呈正相关。多元逐步回归分析表明血清VCAM-1水平是Apelin的独立相关因素。结论胰岛素抵抗大鼠血清Apelin和VCAM-1水平增高,推测Apelin与血管内皮功能受损有关。     

化瘀通脉方对动脉粥样硬化模型兔一氧化氮、内皮素-1表达的影响

目的观察化瘀通脉方对动脉粥样硬化(AS)模型兔一氧化氮(NO)、内皮素(EP)-1表达的影响。方法取雄性健康新西兰大耳白兔40只,随机分为空白组、模型组、对照组、治疗组,每组10只。采用免疫损伤加高脂饲料喂养方法建立新西兰大耳兔AS模型。测定血清NO、血浆ET-1水平。结果实验8 w末,AS兔血清ET-1显著升高,而NO显著降低(P0.05,P0.01)。实验16 w末,治疗组血清ET-1水平较模型组显著降低,NO较模型组显著升高(P0.05,P0.01)。结论化瘀通脉方具有较好的抗AS作用,这可能与其能有效地调节NO/ET-1平衡有关。     

阿托伐他汀对兔主动脉粥样斑块中γ-谷氨酰转移酶表达的影响

目的:研究他汀类药物对于兔主动脉粥样斑块内的γ-谷氨酰转移酶(GGT)表达的影响,同时探讨其表达活性的降低是否有助于斑块的进一步稳定,并证实斑块内的GGT与其他炎性因子的相关性。方法:选取15只新西兰雄性大耳白兔随机分成对照组、高脂组与他汀组。首先通过高脂饮食喂养高脂组和他汀组10周,建立兔主动脉粥样硬化模型。在模型成功建立后,以阿托伐他汀1.5mg·kg-1·d-1连续喂养他汀组6周进行干预。分别于0周、10周末、16周末对实验动物进行TC、TG、LDL、HDL及CRP检测。以ELISA法在第16周末进行GGT-1、VCAM-1和ICAM-1水平检测。实时定量PCR及Western blot方法检测主动脉GGT-1、VCAM-1和ICAM-1的表达。结果:经高脂喂养10周后,高脂组、他汀组兔LDL及TG水平较对照组明显增高,经阿托伐他汀干预治疗6周后他汀组LDL及TG水平较高脂组明显降低[LDL:(11.53±1.87)mmo/L︰(16.87±1.24)mmo/L;TG:(1.68±0.14)∶(2.74±1.88)mmo/L,均P0.05]。各组血CRP水平也有明显差异。相对于对照组,高脂组血浆GGT-1、VCAM-1和ICAM-1水平均显著增高。使用他汀干预后,他汀组兔血浆GGT-1、VCAM-1和ICAM-1水平,主动脉粥样斑块中GGT-1、VCAM-1和ICAM-1表达水平较高脂组均有显著下降(均P0.05)。结论:动脉粥样硬化模型兔外周循环中GGT水平明显升高。使用阿托伐他汀干预治疗后,GGT在其主动脉粥样斑块局部组织中的表达明显下降。阿托伐他汀可以有效抑制斑块中GGT的表达。这可能是他汀类药物抗粥样硬化作用的一个新机制。     

阿托伐他汀对高胆固醇-动脉粥样硬化兔脑组织的抗氧化应激作用研究

目的建立兔高胆固醇-动脉粥样硬化模型，观察阿托伐他汀对脑组织的抗氧化应激保护作用。方法24只健康新西兰白兔随机分为3组：（A组）正常对照组、（B组）高脂饮食组和（C组）高脂饮食加阿托伐他汀组。喂饲8周后，测定兔血清总胆固醇（TC）及低密度脂蛋白（LDL）浓度，取脑组织检测血红素氧合酶（HO-1）水平、超氧化物歧化酶（SOD）活力及丙二醛（MDA）含量的变化。结果ABC三组HO-1平均吸光度值分别为0．418200±0．001874，0．682100±0．001853，0．918800±0．001549；SOD值分别为424．03±14．45、271．79±13．46和402．38±7．35；MDA值分别为16．66±2．55、40．87±2．78和21．57±2．19。与对照组相比，高脂饮食组HO-1表达显著上调，SOD活力下降，MDA含量增加（P〈0．05）；阿托伐他汀组较高脂饮食组HO-1表达进一步上调，SOD活力升高，MDA含量降低（P〈0．05）。结论兔动脉粥样硬化过程中，脑组织处于氧化应激状态，阿托伐他汀可对抗氧化应激损伤，从而减缓动脉粥样硬化的形成。     

动脉粥样硬化实验兔血脂异常对非对称性二甲基精氨酸和C反应蛋白的影响

目的观察高脂饮食复制实验性兔动脉粥样硬化（AS）模型过程中血脂异常对血清非对称性二甲基精氨酸（ADMA）、C反应蛋白（CRP）水平的影响,探讨高脂血症引起AS的可能机制。方法 20只日本大耳白兔给予普通颗粒饲料喂饲1周后,随机分为对照组（普通颗粒饲料喂饲12周）、模型组[高脂饲料（1%胆固醇＋8%猪油＋普通颗粒饲料）喂饲12周]。实验第4、8、12周末取血行生化检测,实验结束后取主动脉全长标本行病理分析。结果与对照组比较,模型组血清TC、TG、LDL-C、CRP、ADMA、内皮素水平增高,NO、HDL-C浓度降低（P〈0.01）。模型组主动脉内膜有不同程度的脂质斑块形成。结论血脂异常可通过炎症反应损伤内皮功能,从而引起AS的形成。     

罗格列酮对兔动脉粥样硬化血脂和组织总抗氧化能力的影响

目的:观察罗格列酮对高胆固醇饮食兔血脂和组织总抗氧化能力的影响,探讨罗格列酮对动脉粥样硬化斑块消退的机制。方法:雄性新西兰大白兔24只随机等分为3组:对照组、胆固醇组、罗格列酮组。罗格列酮从第10周开始干预,16周后,测定血脂、血糖水平,主动脉行病理形态学及颈动脉组织总抗氧化能力的检测。结果:与对照组和胆固醇组相比,16周末时罗格列酮组血清总胆固醇、低密度脂蛋白胆固醇均明显降低;主动脉壁斑块数量和斑块面积显著减少;颈动脉组织总抗氧化能力明显增强。结论:罗格列酮对动脉粥样硬化斑块消退作用的其机制之一可能与降低血清总胆固醇、低密度脂蛋白胆固醇水平及增强组织总抗氧化能力有关。     

补肾宁心方对去势高脂血症家兔主动脉血管细胞粘附分子1表达的调节

为了探讨补肾宁心方对去势雌兔动脉粥样硬化形成的影响及其可能的机制，将26只3月龄新西兰雌兔随机分为正常对照组、假手术组、去势对照组和治疗组(卵巢切除并灌以补肾宁心中药复方)，除正常对照组外均于术后2周给予高脂饮食，治疗组同时灌胃给药，连续3个月。12周末测定血清总胆固醇、甘油三酯、高密度脂蛋白胆固醇和低密度脂蛋白胆固醇水平；取主动脉行组织形态学及扫描电镜观察，并应用免疫组织化学方法检测主动脉血管细胞粘附分子1的蛋白表达。结果发现，与去势对照组比较，补肾宁心方对血脂变化无明显影响，但能明显降低主动脉粥样斑块面积与动脉内膜比值，降低内膜中膜厚度比，减轻主动脉病理损害，抑制主动脉血管细胞粘附分子1的蛋白表达。结果提示，补肾宁心方可能通过抑制主动脉血管细胞粘附分子1的表达从而阻止动脉粥样硬化的发生发展。     

丹红注射液对动脉粥样硬化家兔脂代谢及血管内皮功能的影响

目的观察丹红注射液对动脉粥样硬化(AS)家兔模型脂代谢及血管内皮功能的影响,探讨丹红注射液抗AS作用及可能机制。方法36只新西兰雄性白兔随机均分为正常对照组、高胆固醇组(HC组)、高胆固醇加氟伐他汀组(FC组)和高胆固醇加丹红注射液组(DC组);组织形态学分析AS斑块/内膜面积比值及斑块最厚处内膜厚度/中膜厚度比值;酶法检测血脂;酶法测定血清一氧化氮(NO)和血浆内皮素(ET)水平。结果DC组与HC组比较,血清TC、LDL-C明显降低(P<0.05);血管AS病变显著减轻(P<0.05),血清NO水平显著增高(P<0.05);血浆ET水平显著降低(P<0.05)。结论丹红注射液对实验性AS具有抑制作用,其作用机制可能为①降低血清TC和LDL-C水平,延缓AS斑块的形成;②调节血管内皮细胞生成和释放NO、ET,保护血管内皮细胞功能,进而产生抗AS作用。     

Reduction of serum cholesterol and hypercholesterolemic atherosclerosis in rabbits by secoisolariciresinol diglucoside isolated from flaxseed

BACKGROUND: Secoisolariciresinol diglucoside (SDG) is a plant lignan isolated from flaxseed. Lignans are platelet-activating factor-receptor antagonists that would inhibit the production of oxygen radicals by polymorphonuclear leukocytes. SDG is an antioxidant. Antioxidants studied thus far are known to reduce hypercholesterolemic atherosclerosis. The objective of this study was to determine the effect of SDG on various blood lipid and aortic tissue oxidative stress parameters and on the development of atherosclerosis in rabbits fed a high-cholesterol diet. METHODS AND RESULTS: Rabbits were assigned to 4 groups: group 1, control; group 2, SDG control (15 mg. kg body wt-1. d-1 PO); group 3, 1% cholesterol diet; and group 4, same as group 3 but with added SDG (15 mg. kg body wt-1. d-1 PO). Blood samples were collected before (time 0) and after 4 and 8 weeks of experimental diets for measurement of serum triglycerides, total cholesterol (TC), and LDL, HDL, and VLDL cholesterol (LDL-C, HDL-C, and VLDL-C). The aorta was removed at the end of the protocol for assessment of atherosclerotic plaques; malondialdehyde, an aortic tissue lipid peroxidation product; and aortic tissue chemiluminescence, a marker for antioxidant reserve. Serum TC, LDL-C, and the ratios LDL-C/HDL-C and TC/HDL-C increased in groups 3 and 4 compared with time 0, the increase being smaller in group 4 than in group 3. Serum HDL-C decreased in group 3 and increased in group 4 compared with time 0, but changes were lower in group 3 than in group 4. SDG reduced TC and LDL-C by 33% and 35%, respectively, at week 8 but increased HDL-C significantly, by>140%, as early as week 4. It also decreased TC/LDL-C and LDL-C/HDL-C ratios by approximately 64%. There was an increase in aortic malondialdehyde and chemiluminescence in group 3, and they were lower in group 4 than in group 3. SDG reduced hypercholesterolemic atherosclerosis by 73%. CONCLUSIONS: These results suggest that SDG reduced hypercholesterolemic atherosclerosis and that this effect was associated with a decrease in serum cholesterol, LDL-C, and lipid peroxidation product and an increase in HDL-C and antioxidant reserve.     

Effect of F-1394, an acyl-CoA:cholesterol acyltransferase inhibitor, on atherosclerosis induced by high cholesterol diet in rabbits

Cholesterol-fed rabbits were used to study the anti-atherosclerotic effect of (1S,2S)-2-[3-(2,2-dimethylpropyl)-3-nonylureido]cyclohexane-1-yl 3-[(4R)-N-(2,2,5,5-tetramethyl-1,3-dioxane-4-carbonyl)amino]propionate (F-1394), an acyl-CoA:cholesterol acyltransferase (ACAT) inhibitor. To test its effect on the development of atherosclerosis, rabbits were fed a high-cholesterol diet (HCD) for 6 weeks, followed by regular chow (RC) for 12 weeks plus 0 or 100 mg/kg per day F-1394. Serum total cholesterol (TC) rose to approximately 2000 mg/dl on HCD and then declined gradually after the change in diet in both groups. F-1394 significantly reduced the extent of the atherosclerotic lesions and the total and esterified cholesterol contents of the aorta (by 57,38, and 59%, respectively), without affecting the serum TC level. To clarify whether F-1394 accelerates the regression of preexisting atherosclerosis, rabbits were fed HCD for the first 6 weeks and then RC for the next 6 weeks. Then, the rabbits were given 0 or 100 x 2 mg/kg per day F-1394 for another 12 weeks while on RC. F-1394 significantly reduced the extent of the atherosclerotic lesions and the total and esterified cholesterol content in the aorta (by 31, 31, and 43%, respectively), without affecting the serum TC level. These results demonstrate that F-1394 both prevents the formation of atherosclerosis and accelerates its regression without affecting the serum TC level, indicating that F-1394 acts directly on the arterial wall.     

复方丹参滴丸对动脉粥样硬化粘附因子的作用

目的观察复方丹参滴丸对动脉粥样硬化粘附因子的作用。方法30只雄性新西兰大白兔应用球囊拉伤腹主动脉后,高脂饲养12周,然后随机分为安慰剂组、小剂量复方丹参滴丸组和大剂量复方丹参滴丸组,分别给予安慰剂、复方丹参滴丸5粒/天和复方丹参滴丸10粒/天治疗,12周后处死实验兔,留取腹主动脉标本进行病理检测;实验前后耳缘静脉抽血检测总胆固醇、甘油三酯、低密度胆固醇脂蛋白、高密度脂蛋白和高敏C反应蛋白水平;应用高频超声检测腹主动脉;免疫组织化学染色检测血管细胞粘附因子1和细胞间粘附因子1以及巨噬细胞的分布,逆转录聚合酶链反应检测血管细胞粘附因子1和细胞间粘附因子1mRNA的表达。结果与安慰剂组比较,复方丹参滴丸治疗组可以降低总胆固醇和低密度脂蛋白胆固醇水平(P<0.05),升高高密度脂蛋白胆固醇水平(P<0.05);高敏C反应蛋白有降低趋势;血管细胞粘附因子1、细胞间粘附因子1和巨噬细胞均减少,血管细胞粘附因子1和细胞间粘附因子1mRNA的表达降低(P<0.01);内膜中膜厚度降低(P<0.05)。结论复方丹参滴丸可以抑制粘附因子的表达,从而抑制动脉粥样硬化炎症反应,延缓动脉粥样硬化进展。     

MRI of rabbit atherosclerosis in response to dietary cholesterol lowering.

Direct imaging of the atherosclerotic plaque, rather than the angiographic lumen, may provide greater insight into the response of atherosclerosis to cholesterol-lowering therapy. Aortic plaque was studied in vivo by MRI in rabbits undergoing dietary cholesterol intervention. Thirty-one rabbits underwent aortic balloon injury and high-cholesterol diet for 4 months and then were assigned to low-cholesterol versus continued high-cholesterol diet for up to an additional 16 months. High-resolution (310 micrometer) fast spin-echo MRI of the abdominal aorta was performed at 4, 12, and 20 months and compared with histology. MRI demonstrated a significant reduction in % area stenosis in rabbits placed on low-cholesterol diet (44.6+/-2. 1% at 20 months versus 55.8+/-1.5% at 4 months, P=0.0002). In contrast, % area stenosis increased in rabbits maintained on high-cholesterol diet (69.8+/-3.8% at 20 months versus 55.8+/-1.5% at 4 months, P=0.001). Similarly, plaque thickness decreased significantly in the low-cholesterol group (0.60+/-0.05 mm at 20 months versus 0.85+/-0.06 mm at 4 months, P=0.006), with a trend toward increase in the high-cholesterol group (1.02+/-0.08 mm at 20 months versus 0.85+/-0.06 mm at 4 months, P=0.1). Thus, in rabbits undergoing dietary cholesterol lowering, MRI detected regression of aortic atherosclerotic plaque in vivo. Plaque progression was seen with maintenance of high-cholesterol diet. MRI is a promising noninvasive technology for directly imaging atherosclerosis and its response to therapeutic interventions.     

高脂血症兔主动脉NF-κB、VCAM-1和VEGF的表达及氟伐他汀的影响

目的观察高脂饮食后兔主动脉NF-κB、VCAM－1、VEGF的表达及氟伐他汀的影响，探讨高脂血症引起动脉粥样硬化可能的分子生物学机制和氟伐他汀的作用。方法健康雄性新西兰大耳白兔30只，随机分为5组，高脂饮食4周、6周、8周组，正常饮食和高脂饮食加氟伐他汀组。到规定时间点，处死动物取主动脉标本，观察组织形态学变化，用免疫组化的方法检查NF-κB、VCAM－1和VEGF的表达。结果①高脂血症可以引起NF-κB、VCAM－1、VEGF增加，与对照组比较差异有统计学意义（P〈0．01）。②LDL水平与NF-κB表达呈显著正相关（r=0．922，P〈0．01）；NF-κB与VCAM－1、VEGF呈显著正相关（r＝0．937，P〈0．01，r=0．894，P〈0．01）。③氟伐他汀可以减少NF-κB、VCAM－1和VEGF的表达（P＜0．05）。结论NF-κB、VCAM－1和VEGF参与了动脉粥样硬化的进程，炎症是高脂血症的伴随因素，引起了细胞增殖，与动脉粥样硬化密切相关：氟伐他汀可以减少其表达起到抗动脉粥样硬化作用。     

Attenuation of the development of hypercholesterolemic atherosclerosis by thymoquinone

Thymoquinone (TQ), derived from Nigella sativa seed, is an antioxidant. The present study investigated whether TQ attenuates the development of atherosclerosis, and/or reduces the serum lipid levels and oxidative stress in rabbits. New Zealand white female rabbits were assigned to four groups of six animals each: group I, control; group II, 1% cholesterol diet; group III, 1% cholesterol plus TQ (10 mg/kg/day; through a nasogastric tube) diet; and group IV, 1% cholesterol plus TQ (20 mg/kg/day; through a nasogastric tube) diet. Blood samples were collected at baseline and after four and eight weeks on the experimental diets for measurement of serum lipids, total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), TC/HDL-C ratio and oxidative stress biomarkers (malondialdehyde [MDA] and protein carbonyls). At the end of the eight weeks, the aorta was removed for the assessment of atherosclerotic changes, MDA and protein carbonyls. Group II animals developed atherosclerosis (45%±11% of the intimal surface of aorta was covered with atherosclerotic plaques), which was associated with an increase in the serum TC, TG, LDL-C, HDL-C, TC/HDL-C, MDA and protein carbonyls. In group III, TQ decreased serum TC, LDL-C, MDA and protein carbonyls by 26%, 29%, 85% and 62%, respectively, and aortic MDA by 73%, which was associated with a 40% reduction of the development of aortic atherosclerosis. The higher dose of TQ in group IV had effects similar to the lower dose (group III), except that this dose further decreased serum TG. It is concluded that TQ attenuates hypercholesterolemic atherosclerosis and this effect is associated with a decrease in serum lipids and oxidative stress.