颈动脉内膜增厚/斑块形成与脑梗死的相关性

目的探讨颈动脉内膜增厚/斑块形成不同阶段在脑梗死形成中的作用。方法将2008年2月至2011年2月我科收治的286例缺血性脑血管病患者,经头颅磁共振确定有无新发脑梗死而分为脑梗死组(203例)和非脑梗死组(83例),根据超声检查颈动脉内膜中膜厚度分为正常组(49例)、颈动脉内膜增厚组(39例)和颈动脉斑块形成组(198例);首先观察颈动脉内膜增厚/斑块形成在脑梗死组与非脑梗死组中的分布差异,并进而研究其与脑梗死的相关性。结果脑梗死组具有更高的斑块发生率,非脑梗死组有更多的正常内膜存在,而内膜增厚在两者之间比例相近;以正常内膜组作为参照,Logistic回归分析显示OR(95%CI)在内膜增厚组为2.344(0.971~5.656)、斑块组为3.442(1.797~6.593)。结论颈动脉内膜增厚/斑块形成不同阶段与脑梗死的发生具有不同的致病作用。     

水溶性壳聚糖对腹主动脉球囊损伤大鼠血管狭窄的抑制作用

[摘 要］ 目的:探讨水溶性壳聚糖（WSC）在血管狭窄方面的作用,阐明WSC对大鼠腹主动脉球囊损伤的影响,为开发防治血管狭窄的高效低不良反应药物提供实验依据。方法：75 只雄性 SD大鼠随机分 5 组：50、100和 200 mg/kg 的WSC 组、模型组和对照组（假手术组）,每组15只。采用球囊损伤大鼠腹主动脉内膜方法制备血管狭窄模型,对照组仅分离结扎右髂总动脉。造模后WSC各组经大鼠尾静脉分别注射50、100 和 200 mg/kg浓度的 WSC;模型组和对照组注射生理盐水,每次0.4 mL,每天1次。每组按 7、14 和 21 d 3个时点随机选取 5 只大鼠处死,常规HE染色制作病理切片,观察各组大鼠血管损伤形态,计算相对管腔面积,比较 WSC 对血管狭窄的抑制作用。结果：普通光学显微镜观察,对照组大鼠腹主动脉结构完整,中膜血管平滑肌细胞排列整齐。模型组大鼠在第7天时腹主动脉血管内膜增生明显;第14天时可见内膜、中膜明显增厚,管壁局限性隆起;第21天内膜增厚,以平滑肌细胞为主,中膜细胞排列紊乱,有假腔形成。与模型组比较,实验组第7天时内膜增生明显减轻,以100 和 200 mg/kg WSC组为最好;第14天时可见内膜、中膜增厚均不明显,但200 mg/kgWSC组仍可见大量排列紊乱的血管平滑肌细胞;第21天时各浓度的WSC组均表现正常,其中以200 mg/kg WSC组更为明显。管腔相对面积比较,对照组大鼠管腔面积随术后时间变化不明显（P>0.05）;模型组大鼠管腔面积在第7、14 和 21天时均减小,与对照组比较差异有统计学意义（P<0.01）。50 mg/kgWSC 组大鼠在第 14 天和第21天时,管腔面积有一定的增加,但与对照组比较差异有统计学意义（P<0.01）;100 mg/kg WSC组大鼠的管腔面积明显大于 50 mg/kg WSC 组,其中在第14 天和第21天时的管腔面积与对照组比较差异有统计学意义（P<0.05）;200 mg/kg WSC 组的管腔面积在多于 14 d时为最大,与对照组相比较差异无统计学意义（P>0.05）。各实验组不同天数之间比较差异均无统计学意义（P>0.05）。结论：WSC对大鼠腹主动脉球囊损伤后的血管狭窄有明显抑制作用,其中以200mg/kg浓度的 WSC作用14 d以上为抑制作用最强。     

The inhibitory effect of astilbin on the arteriosclerosis of murine thoracic aorta transplant

The inhibitory effect of astilbin on transplant arteriosclerosis in murine model of thoracic aorta transplantation was examined. Model of rat thoracic aorta transplantation was established. Ninety rats were divided into three groups. In isograft group, the thoracic aorta of Brown Norway （BN） rat was anastomosed with the abdominal aorta of another BN rat. In allograft group, the thoracic aorta of BN rat was anastomosed with the abdominal aorta of Lewis rat. In astilbin group, the rats receiving allo-transplantation were given astilbin 5 mg/kg per day for a time of 28 days. The donor thoracic aorta and the recipient abdominal aorta were anastomosed by means of a polyethylene can- nula （inner diameter： 1.5 mm, length： 3 mm length）. The grafts were histologically examined for structural changes. The areas of arterial lumen and endatrium were calculated. Our results showed that, in the allograft group, 28 days after allografting, conspicuous proliferation of smooth muscles and infiltration with a great number of inflammatory cells were found in the tunica intima and tunica media. Astilbin significantly inhibited the proliferation of smooth muscles and ameliorated the infiltration of inflammatory cells thereyby prevent against the development of transplant arteriosclerosis. It is concluded that asltilbin can effectively prevent the development of arteriosclerosis in allotransplant by inhibiting the proliferation of smooth muscles and inhibit the proliferation of smooth muscles in tunica of intima and media and reducing infiltration of the inflammatory cells.     

Hypertension and Nephrosclerosis: A Reappraisal and a New Theory of Renal Ischemia

An observation in human autopsy material showing a statistically close relationship between complicated atherosclerosis of the aorta, at or above the renal artery take-off, and nephrosclerosis of usual type (i.e. the “granular kidney” of essential hypertension) led to a study of platelet aggregates as a cause of renal lesions. The renal cortical surface is peculiarly sensitive to ischemic damage. When an embolic source, which sheds repeatedly, was placed in the thoracic aorta of rabbits, they became hypertensive. The hypertension persisted for six months, at which time the kidneys showed nephrosclerosis characterized by surface cortical lesions consisting of shrunken glomeruli and atrophical tubules, subtended by arterioles whose intimas showed fibrous thickening. It is suggested that the renal component of the hypertension so induced is transitory, serving as a trigger mechanism for sustained hypertension.     

S108结合丹参对抗异品系大鼠腹主动脉移植硬化的作用

目的　在大鼠腹主动脉移植硬化模型上,探讨Ｓ１０８、丹参对抗移植动脉硬化的作用。方法　大鼠３５ 只随机分为：Ａ组为非移植ＳＤ组,Ｂ组为同品系移植缺血＜ ３０ ｍｉｎ 组,Ｃ 组为异品系移植缺血＜ ３０ ｍｉｎ 对照组,Ｄ组为异品系移植缺血＜３０ ｍｉｎ Ｓ１０８ 加丹参处理组,术后６０ ｄ 切取植入的腹主动脉行光镜、电镜检查,并采用ＭＩＡＳ－ ３００ 计算机图象分析系统,自动测量移植腹主动脉管腔面积、内膜面积及中膜面积。结果　Ｂ组和Ａ组比较,术后６０ ｄ 时动脉内膜未见明显增厚（Ｐ＞０－０５） ,Ｃ组内膜明显增厚（ 与Ａ组、Ｂ组比较,Ｐ＜ ０－０５） 。Ｄ组与Ｃ组比较,内膜增厚有所减轻（Ｐ＜０－０５）。病理观察表明,Ｃ 组、Ｄ 组增生的内膜均由单核／ 巨噬细胞与平滑肌细胞构成。Ｃ组动脉有较严重的细胞浸润,中膜平滑肌细胞坏死,弹力纤维膜断裂。Ｄ 组动脉病理改变明显减轻。结论　Ｓ１０８ 加丹参可以延长异品系大鼠腹主动脉移植硬化的进展。     

高血压患者颈动脉内膜与动脉硬化指数等相关因子变化的临床观察

目的探讨高血压患者颈动脉内膜与动脉硬化指数、血压、血脂、血尿酸、血纤维蛋白原等相关因子的关系,了解高血压合并动脉硬化的原因,为临床判断高血压患者的动脉硬化情况提供依据。方法选取门诊及住院患者中高血压病1、2、3级患者150例,分为颈动脉内膜正常组、增厚组和斑块组三组,观察各组颈动脉内膜中层厚度,动脉硬化指数、血脂、血尿酸、血纤维蛋白原等情况,用统计学的方法进行分析。结果与颈动脉内膜正常组相比较,IMT增厚组和斑块组的动脉硬化指数均升高（P〈0.01）,差异有统计学意义;IMT增厚、斑块形成与高血压的病程、血胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）、血尿酸（UA）、血纤维蛋白原（FIB）呈正相关（P〈0.05）。结论高血压患者随着动脉硬化指数的升高,血管内膜增厚及动脉硬化斑块形成,血中TC、LDL-C、UA、FIB越高,颈动脉内膜越厚且斑块检出率越高。这些因子可作为了解高血压患者动脉硬化程度的指标,作为指导治疗及判断预后的客观标准。     

Intervention of Tongxinluo Capsule (通心络胶囊) against Vascular Lesion of Atherosclerosis and Its Effect on Lectin-like Oxidized Low Density Lipoprotein Receptor-1 Expression in Rabbits

Lectin-like oxidized low-density lipoprotein(ox-LDL) receptor-1 (LOX-1) is a newly identifiedreceptor for cytotoxic ox-LDL in endothelial cellsand plays an i mportant role in the occurrence anddevelopment of atherosclerosis ( AS)(1). Clinicalstudies have showed that Tongxinluo capsule (通心络胶囊,TXL) could alleviate the symptoms of angi-na and myocardial ischemia in patients with coro-nary heart disease.But there werefewstudies con-cerning the effect or therapeutic mechanism of itspreve…     

Intervention of Tongxinluo capsule against vascular lesion of atherosclerosis and its effect on lectin-like oxidized low density lipoprotein receptor-1 expression in rabbits

Objective: To investigate the prevention by Tongxinluo capsule (TXL) of vascular lesions and its effect on the levels of protein and gene expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) of vascular wall in rabbits with atherosclerosis (AS), and to explore its possible mechanism against AS.Methods: AS models were established by feeding New Zealand white rabbits with high-cholesterol diet, and 24 immature rabbits were randomly divided into the control group, model group and treated group (treated with TXL capsule). The indexes of total cholesterol (TO and low density lipoprotein (LDL) levels were measured at the 16th week. The intima thickness and the plaque area of abdominal aorta were quantitatively analyzed by pathological morphological analysis, the expression of macrophage and smooth muscle cell (SMC) in intima were detected by immunohistochemical method and histologic segments were stained by Hematoxilin-Eosin (HE) to identify the degree of atherosclerotic lesion in the model group and the prevention by TXL. The LOX-1 gene and protein expression in abdominal aorta was detected by semi-quantitative RT-PCR and immunohistochemistry, respectively.Results: In the model group, the levels of TC and LDL were significantly elevated, aortic intima thickened extensively, the intima area enhanced, and macrophages expression increased; the levels of LOX-1 gene and protein expression was up-regulated in endothelium and neo-intima of the abdominal aorta. The treatment with TXL reduced blood lipids, attenuated arterial intimai proliferation, markedly inhibited the expression of macrophage and excessively expressed the level of LOX-1.Conclusion: TXL has an inhibitory effect on blood lipids, and it can prevent the occurrence of vascular lesion and cure its development, and its protection against AS was possibly associated with a crucial endothelial protective action through lowering the expression of LOX-1 in vascular walls. Supported by the State Natural Science Foundation of China (No. 30371496).     

急性脑梗死患者外周血炎症指标与颈动脉粥样硬化程度的关系

目的：探讨急性脑梗死患者外周血炎症指标hs-CRP、CD3＋/HLA-DR＋和中性粒细胞CD64指数与颈动脉粥样硬化程度的关系。方法：100例急性脑梗死患者（梗死组）经颈动脉彩色多谱勒超声证实为颈动脉粥样硬化,按病变程度分为颈动脉内膜增厚组（A亚组）20例、颈动脉斑块组（B亚组）56例、颈动脉狭窄组（C亚组）24例,选择50例健康体检者为对照组。采用免疫透射比浊法及流式细胞学检测各组患者外周血hs-CRP、CD3＋/HLA-DR＋和中性粒细胞CD64指数水平,并分析这些指标与颈动脉粥样硬化的关系。结果：梗死组hs-CRP、CD3＋/HLA-DR＋水平均明显高于对照组（P均〈0.01）;且hs-CRP与CD3＋/HLA-DR＋水平呈正相关（Pearsonr=0.408,P〈0.01）。梗死组中性粒细胞CD64指数与对照组比较差异无统计学意义（P〉0.05）。C亚组的hs-CRP、CD3＋/HLA-DR＋水平高于A亚组、B亚组（P均〈0.01）,颈动脉粥样硬化程度与hs-CRP、CD3＋/HLA-DR＋呈正相关（Spearmanrs=0.322,P〈0.01;Spearmanrs=0.387,P〈0.01）。而C亚组的中性粒细胞CD64指数与A亚组、B亚组比较差异无统计学意义。结论：急性脑梗死患者外周血hsCRP、CD3^＋／HLA—DR^＋可在一定程度上反映该患者的颈动脉粥样硬化程度,中性粒细胞CD64指数与颈动脉粥样硬化的关系尚未明确     

气囊导管法与尼龙丝襻法致大鼠颈总动脉内膜增厚模型对比研究

用气囊导管法和尼龙丝襻法分别制成大鼠颈总动脉内膜增厚模型。对比观察动脉壁各层的动脉硬化性改变，特别是中、内膜平滑肌增殖、游走方面的表现；观察到不同程度的动脉中膜平滑肌细胞损伤引起的动脉硬化性病变程度有显著差异。     

辛伐他汀对兔动脉粥样硬化血管平滑肌层GLUT-4mRNA的表达影响

目的观察三羟基三甲基辅酶A(HMG-CoA)还原酶抑制剂—辛伐他汀对兔动脉粥样硬化血管平滑肌层葡萄糖转运蛋白4(GLUT-4)mRNA的表达影响。方法通过高胆固醇喂养建立兔动脉粥样硬化模型,设正常对照组(n=8)、高脂组(n=9)、辛伐他汀组(n=9),第9、20周检测血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)。25周留取兔升主动脉、胸主动脉标本,病理形态学观察升主动脉组织学变化并进行病理形态学定量分析;逆转录多聚酶链式反应测定胸主动脉血管平滑肌层GLUT-4 mRNA的表达。结果高脂饮食诱导兔高胆固醇血症和动脉粥样硬化模型,外周血TC、TG、LDL升高,病理组织学显示内膜(I)/中层(M)厚度比值(I/M)、I M、内膜/中层面积比值(SI/SM)增大,动脉粥样硬化血管平滑肌层GLUT-4表达上调;辛伐他汀组血脂明显降低(P<0.05),I/M、I M以及SI/SM明显减小(P<0.05),同时可抑制GLUT-4 mRNA的表达,与高脂组相比差异有显著性(P<0.05)。结论辛伐他汀早期应用可显著抑制兔动脉粥样硬化的形成,显著降低高胆固醇诱导的兔血脂水平,减少兔动脉粥样硬化血管平滑肌层GLUT-4 mRNA的表达。     

氟伐他汀对高脂血症模型兔血脂的影响及其与内膜增生的关系

为探讨氟伐他汀对血脂的影响及其与内膜增厚的关系 ,将髂动脉内膜剥脱术后高脂血症模型兔随机分为氟伐他汀组和非用药组 (各组n =2 8) ,并设正常对照组 (n =7)。分别于喂高脂饮食前及动脉剥脱术后 1、2、4、8周 ,观察氟伐他汀组和非用药组动物血清TC、TG及LDL C的变化 ;并观察动脉剥脱术后 1、2、4、8周氟伐他汀组和非用药组兔髂动脉切片的新生内膜、中膜厚度及内膜 /中膜比值 (I/M)。结果 :氟伐他汀组血清TC、TG、LDL C浓度明显低于非用药组 (P <0 .0 5) ;氟伐他汀组的新生内膜厚度和I/M明显低于非用药组 (P <0 .0 1 ) ;动脉内膜厚度与TC、TG、LDL C呈明显的直线相关 (偏相关系数分别为 0 .91 1、0 .892、0 .94 2 ,P <0 .0 1 )。提示 :氟伐他汀可调节血脂 ,有效抑制血管内膜过度增生     

内皮剥脱后血管平滑肌增生的时相特征

观察了内皮损伤后血管平滑肌细胞（ＶＳＭＣ）增生的时相变化。结果表明，内皮损伤可导致ＶＳＭＣ增生，内膜增厚。ＶＳＭＣ在术后２４小时就进入细胞周期，开始合成ＤＮＡ；ＤＮＡ复制高峰是在术后４８～７２小时，１０天之后主要是细胞体积增大，细胞外基质堆积，提示细胞的大量复制是在内皮损伤后的早期阶段，这可能是防治的关键时期。     

Elevated peroxidative glutathione redox status in atherosclerotic patients with increased thickness of carotid intima media

Background Atherosclerosis is a chronic inflammatory disease. Accumulated evidences suggest a deep involvement of oxidative damage in the development of atherosclerosis, but little is discussed over the relationship between plasma glutathione redox status as the most important intrinsic antioxidant defensive mechanism and the atherosclerosis. Methods A total of 132 patients suspected with atherosclerosis were assigned to three groups by high frequency ultrasonic examination of the carotid artery. With the thickness of intima of the carotid artery as an index of degree of atherosclerosis progression, 56 were included in plaque-forming group （A）, 42 in carotid artery intima-thickening group （B）, and 34 in normal carotid artery intima-thickness group （C）. All patients were subjected to the measurement of plasma glutathione （GSH） （reduced form GSH and oxidized form GSSG）, nicotinamide adenine dinucleotide phosphate （NADP） （reduced form NADPH and oxidized form NADP^＋）, oxidized low density lipoprotein （oxLDL）, and malondialdehyde （MDA） The GSH/GSSG and NADPH/NADP^＋ redox potentials were calculated according to the Nernst equation, and their correlation with intima thickness and oxLDL was analyzed. Results With the thickening of artery intima （from group C to A）, GSH concentration and the ratio of GSH/GSSG gradually reduced, and GSSG and GSH/GSSG redox potential gradually increased （more positive） （P 〈0.05）. The NADPH and NADPH/NADP^＋ redox status also showed similar but milder changes. The products of oxidative stress oxLDL and MDA increased significantly along with the thickening of artery intima （P 〈0.05）. The analysis of the relationship between GSH/GSSG redox potential, intima thickness, and oxLDL showed positive correlations （P 〈0.05）. The plasma GSH/GSSG redox status was positively correlated with the intima thickness of the carotid artery and the oxidized injury of LDL. The redox status shifted to oxidizing direction along with the intima thickening and plaque-forming. Conclusion Elevated peroxidative glutathione redox status was deeply implicated in atherosclerosis progressing, and it may be a sensitive and reliable index for monitoring oxidative status in atherosclerosis.     

小檗碱联合辛伐他汀对动脉粥样硬化模型大鼠的抗动脉粥样硬化作用及其机制

目的：探讨小檗碱联合辛伐他汀对动脉粥样硬化（AS）模型大鼠胸主动脉组织中血管内皮生长因子（VEGF）、转化生长因子β1（TGF-β1）、白细胞介素18（IL-18）和白细胞介素10（IL-10）表达的影响,阐明小檗碱联合辛伐他汀抗动脉硬化的作用机制。方法：48只大鼠随机分为对照组,模型组,辛伐他汀组,低、中和高剂量小檗碱联合辛伐他汀组,每组8只。给药4周后取大鼠血清和胸主动脉组织,HE染色法观察各组大鼠胸主动脉组织病理形态表现,双抗体夹心ABC-ELISA法检测各组大鼠血清中VEGF、TGF-β1、IL-18和IL-10水平,全自动生物化学分析仪测定各组大鼠血清总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白（LDL-C）和高密度脂蛋白（HDL-C）水平,免疫组织化学法检测各组大鼠胸主动脉组织中VEGF、TGF-β1、IL-18和IL-10蛋白表达水平。结果：HE染色,与对照组比较,模型组大鼠主动脉内膜明显增厚、细胞内外有脂质沉积,内膜下可见坏死物沉积,内壁出现斑块、不平整,血管腔狭窄;与模型组比较,高剂量小檗碱联合辛伐他汀组大鼠动脉血管壁无明显斑块出现,内膜增厚不平整明显改善。与模型组比较,辛伐他汀组和不同剂量小檗碱联合辛伐他汀组大鼠血清中TC、TG和LDL-C水平明显降低（P<0.05或P<0.01）,HDL-C水平明显升高（P<0.05）。ABC-ELISA法检测,与模型组比较,辛伐他汀组和不同剂量小檗碱联合辛伐他汀组大鼠血清中VEGF和IL-18水平均降低（P<0.05或P<0.01）,TGF-β1和IL-10水平升高（P<0.05）。免疫组织化学法检测,与模型组比较,辛伐他汀组大鼠胸主动脉组织中IL-18蛋白表达水平明显降低（P<0.05）,TGF-β1蛋白表达水平明显升高（P<0.05）;不同剂量小檗碱联合辛伐他汀组大鼠胸主动脉组织中VEGF和IL-18蛋白表达水平均明显降低（P<0.05）,TGF-β1和IL-10蛋白表达水平明显升高（P<0.05）。结论：小檗碱联合辛伐他汀能通过下调小鼠血清和胸主动脉组织中VEGF和IL-18蛋白表达水平,上调TGF-β1和IL-10蛋白表达水平,发挥抗AS作用。     

广西南宁地区年轻人主动脉内膜嗜苏丹病变的形态定量研究

应用图像分析仪对１２０例１５～３９岁广西人主动脉内膜的嗜苏丹病变（ＳＬ）进行了测试，建立ＳＬ的发生概率图。结果表明，ＳＬ的检出率为１００％；ＳＬ的面积百分比在２５～２９岁组最大；ＳＬ的发生率在血管分枝开口周围最高，并且后壁较前壁高，侧壁又较前壁高。     

实验性糖尿病与动脉粥样硬化关系的研究

本实验采用形态与功能相结合的方法,观察分析糖尿病大鼠及其加饲动脉粥样硬化饮食大鼠主动脉的形态学变化。结果表明,实验性糖尿病对饲动脉粥样硬化饮食大鼠主动脉病变的形成无阻碍作用,而且能增加其病变发生的敏感性。同时认为,脂质代谢紊乱以及血清过氧化脂质异常可能与糖尿病时血管病变的形成密切相关。     

高血压左室肥厚的消退与冠状动脉血流储备改善的关系

目的　探讨高血压左室肥厚 (LVH)的消退与冠脉血流储备 (CFR)的关系。方法　将 96例高血压合并左室肥厚的患者分入雷米普利、氯沙坦和联合用药组 ,治疗 6个月后 ,采用多平面经食管超声心动图和动态三维超声心动图评价用药前后左室重量 (LVM)和CFR的变化。结果　治疗 6个月后 ,雷米普利组、氯沙坦组及联合用药组收缩压、舒张压均显著下降 ,LVM明显减轻 (P均 <0 0 1) ;雷米普利组、氯沙坦组及联合用药组治疗后 ,经LVM校正的CFR指标 :静脉注射双密达莫后与基础状态下舒张期流速时间积分比 (D/RDviC)均较治疗前显著增加 ( 1 83± 0 6 1vs 1 5 7± 0 5 8,P <0 0 5 ;1 94± 0 45vs 1 5 3± 0 6 4,P <0 0 1;2 0 3± 0 38vs 1 49± 0 34,P <0 0 1) ;D/RDViC 的改变与LVM的减轻呈显著正相关 (r=0 5 79,P <0 0 1) ,与SBP、DBP的降低无显著相关性 (r分别为 0 2 88和 0 2 95 ,P均 >0 0 5 )。结论　雷米普利、氯沙坦单用或者合用均显著降压、减轻心肌肥厚 ,改善CFR ,并且LVH的消退与CFR的改善密切相关。     

有氧运动对高脂血症大鼠血脂的影响及其机制

目的 探讨有氧运动对高脂血症大鼠血脂的影响及其作用机制。方法 将120只8周龄健康雄性SD大鼠随机分为正常对照组、高脂饮食组、SBC-115076组和有氧运动组,每组30只。正常对照组饲喂标准饲料,其余3组饲喂高脂饲料构建大鼠高脂血症模型;SBC-115076组每周注射前蛋白转化酶枯草溶菌素9（PCSK9）抑制剂SBC-115076（8 mg/kg）1次,连续8周;有氧运动组进行无负重游泳,每周6 d,共持续8周。8周后处死大鼠,采集血液标本,测定血清三酰甘油（TG）、总胆固醇（TC）、低密度脂蛋白（LDL）、高密度脂蛋白（HDL）水平。取胸主动脉标本,经H-E染色观察主动脉病理学改变。取肝组织标本,采用实时荧光定量PCR、蛋白质印迹分析和免疫荧光法检测肝组织中PCSK9、低密度脂蛋白受体（LDLR）和胆固醇调节元件结合蛋白（SREBP）在mRNA和蛋白水平的表达。结果 高脂饮食组大鼠血清TG、TC和LDL水平高于对照组,HDL水平低于对照组（P<0.01）;SBC-115076组和有氧运动组大鼠血清TG、TC、LDL水平低于高脂饮食组,HDL水平高于高脂饮食组（P<0.01）。高脂饮食组大鼠主动脉壁内膜增厚,内皮细胞损伤脱落;与高脂饮食组相比,有氧运动组大鼠主动脉内膜增厚明显减轻,内皮损伤较少。与对照组相比,高脂饮食组大鼠肝组织中PCSK9、SREBP1和SREBP2的mRNA及蛋白表达水平升高,LDLR的mRNA及蛋白表达水平降低（P<0.01）;与高脂饮食组相比,SBC-115076组和有氧运动组大鼠肝组织中PCSK9、SREBP1和SREBP2的mRNA及蛋白表达水平降低,LDLR的mRNA及蛋白表达水平升高（P<0.01）。结论 有氧运动能降低高脂血症大鼠血清TG、TC和LDL水平,升高HDL水平,并减轻主动脉内膜增厚。其机制可能与降低PCSK9和SREBP蛋白的表达,从而解除对LDLR的抑制有关。