Vit E对动脉粥样硬化模型兔动脉肌球蛋白轻链激酶表达的影响

目的　研究动脉粥样硬化 (AS)模型兔动脉肌球蛋白轻链激酶表达的变化以及VitE对MLCK表达的影响。方法　复制AS兔模型 ;颈动脉取血后检测血清标本中各种血脂成分的变化 ,用免疫组化法和Westernblot分析动脉粥样硬化模型兔动脉MLCK的表达。结果　成功建立AS兔模型 ,模型血清中各种脂质发生显著变化。免疫组化和West ernblot实验表明 ,动脉粥样硬化模型兔在喂食胆固醇膳食 4wk和 12wk后动脉MLCK的表达增强 ,在喂食胆固醇膳食12wk同时添加VitE时 ,MLCK表达降低。结论　AS模型兔动脉MLCK的表达增强与动脉粥样硬化的形成相关。VitE可能是降低动脉MLCK表达的因素 ,同时抑制动脉粥样硬化的形成。     

褪黑素对动脉粥样硬化模型兔动脉肌球蛋白轻链激酶表达及活性的影响

目的探讨褪黑素(melatonin,MLT)对动脉粥样硬化模型兔动脉肌球蛋白轻链激酶(MLCK)表达与活性的影响。方法复制动脉粥样硬化兔模型,采用免疫组化和Western blot分析主动脉MLCK蛋白表达,γ-32P-ATP参入法检测MLCK活性。结果成功建立动脉粥样硬化兔模型,高脂喂食12wk,兔主动脉MLCK蛋白表达水平增加,活性上升,经MLT治疗后动脉粥样硬化斑块减少,MLCK蛋白表达下降,活性下降。结论动脉粥样硬化的形成与MLCK蛋白表达与活性升高有关,MLT能降低动脉MLCK蛋白表达和活性。     

培哚普利对胰岛素抵抗的影响

目的 :研究培哚普利对胰岛素抵抗高血压大鼠胰岛素抵抗 (IR)的影响。方法 :选择雄性SD大鼠 30只分成 2组 ,对照组饲以基础饲料 ,培哚普利组饲以高糖高盐饲料 ,4wk后用培哚普利 0 .8mg·kg- 1·d- 1灌胃 4wk ,观察 2组实验前、4wk、8wk时收缩压 (SBP)、空腹血糖 (FBG )、空腹血胰岛素 (FINS)、胰岛素敏感性指数 (ISI)及红细胞膜Na ,K ATP酶活性测定的变化。结果 :培哚普利组 4wk时SBP升高 ,上升值为 (4 .4±s 1.6 )kPa ,FBG上升值 (0 .4± 0 .3)mmol·L- 1,FINS升高 (12 .7±2 .1) μU·L- 1,ISI降低 ,差值 1.30± 0 .2 0 ,红细胞膜Na ,K ATP酶活性降低 (12± 6 )nmoL·pi·mg- 1·pro·h- 1,P <0 .0 1。 8wk与 4wk时比较分别为 ,SBP[(13.2± 1.2 )kPavs (17.0± 2 .0 )kPa](P <0 .0 1) ,FBG分别为 [(2 .9± 0 .7)mmol·L- 1vs (3.8± 0 .3)mmol·L- 1](P <0 .0 1) ,FINS分别为 [(8.0± 1.5 ) μU·L- 1vs (18± 3) μU·L- 1](P <0 .0 1) ,ISI分别为 [(- 3.2 0± 0 .2 0 )vs (- 4.2 0± 0 .2 0 ) ](P <0 .0 1) ,红细胞膜Na ,K ATP酶活性分别为[(36± 9)nmoL·pi·mg- 1·pro·h- 1vs (2 6± 6 )nmoL·pi·mg- 1·pro·h- 1](P <0 .0 1)。结论 :培哚普利能改善高糖高盐饲养大鼠的IR。     

醋氨己酸锌治疗胃溃疡的作用机制的探讨

目的 :测定胃溃疡病人胃粘膜中前列腺素E2 (PGE2 )、氨基己糖含量 ,以探讨醋氨己酸锌治疗胃溃疡的作用机制。方法 :12 4例病人分为对照组60例 ,给予奥美拉唑 2 0mg ,每晨 1次口服 ,共 4wk ,同时服用阿莫西林 1g ,bid ,甲硝唑 0 .4 g ,bid ,共 1wk ;治疗组 64例 ,除同样服用上述 3种药物外 ,加服醋氨己酸锌 30 0mg ,tid ,4wk为一个疗程。结果 :治疗组胃溃疡治愈率 ( 94 %)明显优于对照组 ( 80 %) ,P <0 .0 5。治疗组治疗后PGE2 含量为 ( 2 .8±s 0 .6) μg·mg- 1组织 ,明显高于治疗前[( 1.4± 0 .3) μg·mg- 1组织 ](P <0 .0 1) ,而对照组则无明显变化 ,分别为 ( 1.4± 0 .4 ) μg·mg- 1组织和( 1.4± 0 .3) μg·mg- 1组织。治疗组治疗后氨基己糖水平为 ( 18.6± 2 .6) μg·mg- 1组织 ,明显高于治疗前[( 14.2± 2 .4 ) μg·mg- 1组织 ],P <0 .0 1,而对照组则无明显变化 ,分别为 ( 14.4± 2 .5 ) μg·mg- 1组织和( 15± 4 ) μg·mg- 1组织。结论 :醋氨己酸锌可提高胃粘膜中PGE2 、氨基己糖含量 ,减轻胃粘膜损伤 ,促进胃溃疡愈合。     

硫化氢供体对Apo E基因敲除小鼠动脉粥样硬化的调节作用

目的探讨硫化氢(H2S)供体对Apo E基因敲除小鼠(Apo E-/-)动脉粥样硬化的调节作用。方法6wk龄正常C57BL/6J和Apo E-/-小鼠分为正常对照组、ApoE-/-组和Apo E-/-+硫氢化钠(NaHS)组,每组各8只,普通饮食饲养至16wk龄。分别观察各组小鼠血清中总胆固醇(TCHO)、低密度脂蛋白(LDL-C)和高密度脂蛋白(HDL-C)含量及主动脉根部斑块面积的变化;用硫电极法测定血清中H2S的含量。结果与对照组相比,Apo E-/-小鼠血清中TCHO[(12.59±3.11vs2.32±0.40)μmol·L-1]和LDL-C[(1.33±0.43vs0.13±0.03)μmol·L-1]水平明显升高,而HDL-C水平[(0.45±0.13vs1.49±0.21)μmol·L-1]明显降低,血清中H2S的含量[(44.64±4.52)μmol·L-1]较对照组[(57.69±7.03)μmol·L-1]明显下降,主动脉根部明显出现斑块[(139316.6±30362.93vs0)μm2];给予NaHS后,Apo E-/-小鼠血清中TCHO、LDL-C和HDL-C水平无明显变化,而血清中H2S的含量明显升高[(52.21±7.24vs44.64±4.52)μmol·L-1],主动脉根部动脉粥样硬化斑块明显缩小[(85927.84±1922.73vs139316.6±30362.93)μm2]。结论新型气体信号分子H2S可以延缓动脉粥样硬化的进程,缩小动脉粥样硬化斑块形成。     

螺旋藻对大鼠实验性肝纤维化的预防作用

目的 :研究螺旋藻对大鼠实验性肝纤维化的预防作用。方法 :实验分正常对照组、四氯化碳组、螺旋藻组 (均n =8)。后 2组分别用 4 0 %四氯化碳 (橄榄油溶液 )制备大鼠肝纤维化模型 ,螺旋藻组给予含螺旋藻精粉的指状饲料条 ,共 12wk。观察肝脏组织学、肝羟脯氨酸 (HYP)含量、血清PC Ⅲ及HA水平。结果 :螺旋藻组肝纤维化程度明显轻于四氯化碳组 ,螺旋藻组PC Ⅲ [(140±s 37) μg·L- 1]和HA[(2 6 2± 92 ) μg·L- 1]显著低于四氯化碳组 [(2 74± 6 9) μg·L- 1]和 [(4 84± 114) μg·L- 1](P<0 .0 1) ,肝HYP含量螺旋藻组 [(174± 37) μg·g- 1]亦显著低于四氯化碳组 [(2 4 3± 4 9) μg·g- 1](P <0 .0 5)。结论 :螺旋藻对实验性肝纤维化有预防作用。     

中、低热量饮食,中等量运动和二甲双胍治疗青少年肥胖病人初探

目的 :探讨中、低热量饮食 ,中等量运动和二甲双胍治疗青少年肥胖的疗效。方法 :2 4例单纯性肥胖青少年志愿者 ,随机分为A ,B 2组。A组 1～ 8wk和B组 17～ 2 4wk服用二甲双胍 0 .2 5 g ,tid ;B组 1～ 8wk和A组 17～ 2 4wk服用安慰剂 1片 ,tid。结果 :A ,B 2组病人治疗前后的BMI分别为 (35±s 9vs 2 6± 6;35± 9vs 2 5± 6)kg·m- 2 ,WHR (1.0 2± 0 .10vs 0 .84± 0 .0 6;1.0 1± 0 .0 8vs0 .84± 0 .0 6) ,Fins[(80± 2 1) ,(5 9± 14) ;(80± 2 3) ,(5 4± 13)mU·L- 1],TG[(3.8± 1.6) ,(1.8± 1.0 ) ;(3.9± 1.5 ) ,(1.6± 0 .9)mmol·L- 1],TC[(6.8±2 .1) ,(5 .0± 1.1) ;(6.9± 2 .1) ,(5 .0± 1.7)mmol·L- 1],BUA[(4 93± 132 ) ,(35 6± 79) ;(4 91± 15 3) ,(378± 10 6) μmol·L- 1]和γ GT [(5 2± 13) ,(32±10 ) ;(5 1± 12 ) ,(32± 10 )U·L- 1]均明显降低 (均P<0 .0 5 ) ;A组 1～ 8wk服用二甲双胍时BMI ,WHR ,FIns ,TG ,γ GT的降低较B组更明显 ,而B组 17～ 2 4wk加用二甲双胍后与A组的差异消失。结论 :中、低热量饮食 ,中等量运动和二甲双胍对青少年肥胖病人有一定治疗作用     

氯沙坦对肾缺血再灌注大鼠肾组织超氧化物歧化酶和丙二醛的影响

目的 :探讨氯沙坦干预急性肾缺血再灌注损伤的保护机制。方法 :实验大鼠分正常组、假手术组、缺血再灌注模型组、氯沙坦组 (预先喂服氯沙坦 )。检测各组在急性肾缺血 1h、再灌注 1h和 2 4h肾组织匀浆中超氧化物歧化酶 (SOD)活力与丙二醛 (MDA )含量变化。结果 :模型组和氯沙坦组MDA含量与正常组和假手术组比较均显著增高 (P<0 .0 1) ;氯沙坦组在再灌注 1h和 2 4h ,MDA含量(7.7± 1.0 )nmol·mg- 1pro和 (9.2± 0 .5 )nmol·mg- 1pro较模型组 (9.5± 0 .4 )nmol·mg- 1pro和(11.9± 0 .9)nmol·mg- 1pro明显降低 (P <0 .0 5 )。模型组与正常组和假手术组比较SOD活力明显降低 (P <0 .0 5 ) ;氯沙坦组在缺血 1h ,再灌注 1h和2 4h ,SOD活力分别为 (81.3± 1.6 )NU·mg- 1pro ,(79± 4 )NU·mg- 1pro和 (48± 4 )NU·mg- 1pro)较模型组 (6 8± 8)NU·mg- 1pro ,(48± 11)NU·mg- 1pro和 (18± 4 )NU·mg- 1pro明显增高 (P <0 .0 5 )。结论 :氯沙坦能减轻急性肾缺血再灌注时氧自由基引起的损伤     

硝酸异山梨酯静脉滴注对冠心病病人血管内皮功能的影响

目的 :观察硝酸异山梨酯静脉滴注对冠心病病人血管内皮功能的影响。方法 :6 4例冠心病病人随机分为 2组 ,硝酸异山梨酯组 (32例 )予硝酸异山梨酯 2 0mg ,iv ,gtt,qd ;复方丹参组 (32例 )予复方丹参 2 0mL ,iv ,gtt ,qd。均连续用药 4wk。结果 :硝酸异山梨酯组治疗后 6 酮前列腺素F1α(99± 6 9)ng·L- 1]、一氧化氮 [(134± 88) μmol·L- 1]均较治疗前 [(75± 5 8)ng·L- 1,(91± 85 ) μmol·L- 1]上升 ,血组织型纤溶酶原激活物抑制物 [(0 .6 4± 0 .2 7)×10 3AU·L- 1vs (0 .5 4± 0 .2 4 )× 10 3AU·L- 1]、凝血烷B2 [(111± 2 31)ng·L- 1vs (71± 14 6 )ng·L- 1]、内皮素 1[(98± 6 2 )ng·L- 1vs (80± 4 7)ng·L- 1],浓度均下降 (P <0 .0 5 ,P <0 .0 1)。复方丹参组无此变化 (P >0 .0 5 )。结论 :硝酸异山梨酯静脉滴注可改善冠心病病人血管内皮功能     

百草降脂灵对动脉粥样硬化兔OX-LDL和LDL-RmRNA表达的影响

目的 :研究百草降脂灵预防性给药对动脉粥样硬化 (atherosclerosis,AS)兔氧化低密度脂蛋白(OX LDL)、低密度脂蛋白受体 (LDL R)mRNA表达的影响。方法 :用 4F (Forgarty)导管拉伤兔腹主动脉内皮 ,然后连续喂饲高脂饲料 ,6wk后造成兔AS模型。同时预防性给予百草降脂灵 0 .1 6g·kg-1,0 .3 2 g·kg-1,1 2wk后取兔腹主动脉 ,采用DAB显色法 ,研究各组间OX LDL表达情况。另取兔肝脏 ,利用RT PCR技术研究百草降脂灵预防性给药后对LDL RmRNA表达的影响。结果 :百草降脂灵组同AS模型组相比 ,兔腹主动脉OX LDL表达明显降低 (P <0 .0 5或P <0 .0 1 ) ,兔肝脏LDL RmRNA表达明显增加 (P <0 .0 1 )。结论 :百草降脂灵预防性给药可减少兔腹主动脉OX LDL表达 ,增加兔肝脏LDL RmRNA表达 ,这是百草降脂灵预防兔动脉粥样硬化发生发展的可能机制之一。     

Oren-gedoku-to and Keishi-bukuryo-gan-ryo inhibit the progression of atherosclerosis in diet-induced hypercholesterolemic rabbits

In this study, we examined whether the Kampo formulas Oren-gedoku-to (OGT, Huanglian-jie-du-tang in Chinese) and Keishi-bukuryo-gan-ryo (KBG, Gui-zhi-fu-ling-wan in Chinese) could prevent the progression of atherosclerosis in cholesterol-fed rabbit, an animal model for hypercholesterolemia in vivo. Twenty-four male Japanese white rabbits (2 kg body weight) were divided into four groups. The control group was fed standard rabbit chow containing 1% cholesterol, the OGT group was fed standard rabbit chow containing 1% cholesterol and 1% OGT, the KBG group was fed standard rabbit chow containing 1% cholesterol and 1% KBG, and the vitamin E group was fed standard rabbit chow containing 1% cholesterol and vitamin E (450 mg/1000 g). All four groups were kept on these diets for 8 weeks. At the end of the experiments, the percentage of surface area of the total thoracic aorta with visible plaque was significantly reduced in the OGT and KBG groups. The serum thiobarbituric acid reactive substances of the vitamin E group showed a significantly low value compared with the control group, whereas the serum lipid peroxide levels of the OGT and KBG groups were considerably lower than that of the control groups as well as that of the vitamin E group. Furthermore, the urinary 8-hydroxydeoxyguanosine levels of the OGT and KBG groups were considerably lower than that of the vitamin E group. These results suggest that OGT and KBG prevent the progression of atheromatous plaque by creating a sounder antioxidant defense system than vitamin E.     

Experimental hyperlipidemia and atherosclerosis induced by cholesterol diet in SPF Japanese white rabbits

Experimental hyperlipidemia and atherosclerosis induced by a cholesterol diet in SPF male and female rabbits (JW/KBL) were investigated by the determination of the lipid contents of the plasma, liver and thoracic aorta; determination of morphological changes of the aortic arch by head angiography; and computer tomography of the brain. Rabbits were fed the diet that contained 1% cholesterol for eight weeks. The plasma lipid levels began to rise from two weeks after the cholesterol diet was started, reached the peak four to six weeks later, and then fell in both males and females at eight weeks. The cholesterol of the high density lipoprotein in male rabbit plasma was slightly increased by the cholesterol diet, but not in female rabbits. An increase in the total cholesterol (TC) and triglyceride contents of the liver and an increase in the TC and phospholipid contents of the thoracic aorta were observed at the eighth week. Histological examination of the aortic arch showed marked lipid vacuoles under the endothelial cells, noticeable lipid inclusions in the smooth muscle cells of the intima and granular prominences on the internal surface of the aorta. Head angiography of rabbits fed the cholesterol diet revealed a constriction of the lumina of several arteries due to the lipid depositions. These results suggest that hyperlipidemia and atherosclerosis can be produced at the eighth week using SPF rabbits fed on a cholesterol diet.     

葡萄籽原花青素对动脉粥样硬化兔血脂的调节作用

目的　研究葡萄籽原花青素 (GSP)对动脉粥样硬化(AS)兔血脂的调节作用。方法　 2 4只♂新西兰大白兔随机分为正常对照 (A)组、高脂模型 (B)组、GSP预防干预 (C)组 ,分别饲喂标准、标准 + 1%胆固醇、标准 + 1%胆固醇 + 1%GSP的颗粒饲料 ,于实验开始前 1d和开始后第 1、2、4、8、12wk末取空腹血 ,检测血清甘油三酯 (TG)、总胆固醇 (TC )、高密度脂蛋白胆固醇 (HDL C)、低密度脂蛋白胆固醇 (LDL C)。 12wk末取血后处死 ,取主动脉作病理形态学观察。所有数据经SAS 8 2进行混合模型的变异数分析。结果　与B组比较 ,C组TC、LDL C、TG和TG/HDL C在 12wk时降低 (P <0 0 1) ,HDL C升高 (P <0 0 5)。病理分析显示C组兔主动脉壁厚度和泡沫细胞数量明显较B组减轻 (P <0 0 1)。结论　GSP对血脂有调节作用 ,可通过降低TC、LDL C、TG、TG/HDL C和升高HDL C的作用而发挥抗AS作用 ,并有可能改善胰岛素抵抗状态     

Early benefits of pravastatin to experimentally induced atherosclerosis

There is little information regarding the time of hypolipidemic treatment of changes in atherosclerotic plaque, tissue cholesterol content, and also for the recovery of endothelial function. To assess the early effects of lipid-lowering treatment on these parameters, six groups of New Zealand male rabbits were studied. Animals in groups I and II were fed regular chow; groups III and IV received a 12-week 0.5% cholesterol diet followed by 12 weeks of 0.05% cholesterol diet. Finally, groups V and VI were fed a 12-week 0.5% cholesterol diet and were then shifted to a regular diet for 12 weeks. During the last four weeks, the rabbits in groups I, III, and V received low-dose pravastatin (2 mg/day), added to the diet. Group IV animals had the highest cholesterol plasma levels (vs. groups I, II, III, and V, p < 0.01) and presented atherosclerotic plaques in a more advanced stage. Nonatherogenic diet was insufficient to restore endothelial function in animals previously fed cholesterol-enriched diets (groups IV and VI). Conversely, pravastatin treatment promoted significant improvement in endothelial function and reduced the progression of atherosclerosis. Marked increase in cholesterol content was seen in aorta and liver in response to the atherogenic diet. However, neither treatment with pravastatin nor nonatherogenic diet was capable of modifying the tissue cholesterol content. Our study supports the hypothesis that the early use of statins can attenuate the progression of atherosclerosis and ameliorate endothelial function. In addition, significant changes in the tissue cholesterol pool probably need a longer period of treatment.     

黄芪总黄酮对动脉粥样硬化早期形成的影响

目的 探讨黄芪总黄酮(TFA)对高脂饲料诱导家兔动脉粥样硬化(AS)的防护作用。方法 60只新西兰白兔被随机分为5组,分别给正常饲料(对照组,n=10)、高脂饲料(造模组,n=10)、高脂饲料加维生素E 400 IU·d~(-1)(VitE组,n=10)、高脂饲料加TFA 60 mg·d~(-1)(TFA 1组,n=15)和高脂饲料加TFA 120 mg·d~(-1)(TFA 2组,n=15)处理12 wk,动态监测(0、8和12 wk)血脂的变化,实验结束前,所有动物用CO_2处死,分别检测主动脉弓的病理变化和胆固醇的含量。结果 实验数据表明所有接受高脂饲料的动物血浆中的总胆固醇、甘油三脂、主动脉弓的粥样硬化斑块面积、胆固醇含量和动脉壁内膜与中膜平均厚度比值均高于正常饲料组。TFA能降低血浆总胆固醇(P<0.05)、动脉壁中的胆固醇和动脉壁内膜与中膜比率;两种浓度的TFA(60和120 mg·d~(-1))能分别降低43.1％和63.0％的AS斑块面积;维生素E可降低动脉壁中的胆固醇沉积和动脉壁内膜与中膜比率(P<0.05),减低43.7％的AS斑块面积。在本实验中TFA和维生素E对甘油三脂代谢无影响。结论 TFA对高脂饲料诱导家兔AS形成有一定的防护作用。     

Naringin has an antiatherogenic effect with the inhibition of intercellular adhesion molecule-1 in hypercholesterolemic rabbits.

Naringin, a bioflavonoid found in citrus fruit peel, is known to have an antioxidative effect, but its effect on atherosclerosis has not been studied. This study evaluated the effect of naringin on blood lipid levels and aortic fatty streaks, and its action mechanism in hypercholesterolemic rabbits. Male New Zealand white rabbits were fed a 0.25% cholesterol diet and divided into an untreated group (n = 4), a naringin-treated group (n = 5; 500 mg/kg per day), and a lovastatin-treated group (n = 5; 20 mg/kg per day). After 8 weeks, blood was sampled and analyzed biochemically. Aorta and liver were harvested and examined histologically. Cholesterol level in rabbits fed the 0.25% cholesterol diet reached 17 times normal and decreased in the rabbits fed naringin and lovastatin, whose effects were not statistically significant (p > 0.05). However, both naringin and lovastatin effectively decreased the area of fatty streak in thoracic aorta on macroscopic analysis (p < 0.05) and significantly reduced subintimal foam cell infiltration on microscopic morphometry (p < 0.05). These foam cells were macrophages on immunohistochemical analysis. Naringin treatment inhibited hypercholesterolemia-induced intercellular adhesion molecule-1 (ICAM-1) expression on endothelial cells. Hypercholesterolemia caused fatty liver and elevation of liver enzymes, which was prevented by naringin but not by lovastatin. Naringin significantly reduced fatty streak formation and neointimal macrophage infiltration and also inhibited the expression of ICAM-1 in endothelial cells, suggesting that suppression of ICAM-1 contributed to the antiatherogenic effect. Naringin, unlike lovastatin, has a hepatoprotective action.     

Effect of vitamin E on the development of atherosclerosis

The development of atherosclerosis is a multifactorial process in which both elevated plasma cholesterol levels and proliferation of smooth muscle cells play a central role. Numerous studies have suggested the involvement of oxidative processes in the pathogenesis of atherosclerosis and especially of oxidised low density lipoproteins. Some epidemiological studies have shown an association between high dietary intake or high serum concentrations of vitamin E and lower rates of ischemic heart disease. Recently, the Cambridge Heart Antioxidant Study (CHAOS) reported strong protection by high vitamin E doses against the risk of fatal and non fatal myocardial infarction. Here we have shown that incubation of vascular smooth muscle cells in the presence of alpha-tocopherol resulted in inhibition of cell proliferation and protein kinase C activity. Since beta-tocopherol and probucol are not inhibitory, the effect of alpha-tocopherol is considered due to a non-oxidant mechanism. In order to understand the protective role of alpha-tocopherol against atherosclerosis in vivo the following rabbit studies were carried out. Atherosclerosis was induced by a vitamin E poor diet containing 2% cholesterol in a group of rabbit. The other groups had 2% cholesterol in the diet plus 50 mg/kg vitamin E i.m. or 1% probucol or 50 mg/kg vitamin E plus 1% probucol. After 4 weeks, aortas were removed and analysed by microscopy for atherosclerotic lesions. Samples of the media were analysed for protein kinase C activity. The aortas of cholesterol-fed rabbits showed typical atherosclerotic lesions, detected by microscopic examination, their media smooth muscle cells exhibited an increase in protein kinase C activity. Vitamin E fully prevented cholesterol induced atherosclerotic lesions and the induction of protein kinase C activity while probucol was not effective. These results show that the protective effect of vitamin E against hypercholesterolemic atherosclerosis is not produced by an other antioxidant such as probucol and, therefore, may not be linked to the antioxidant properties of this vitamin. The effects observed at the level of smooth muscle cells in vitro and ex-vivo suggests an involvement of signal transduction events in the protective effect of vitamin E against atherosclerosis.