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1.
目的:检测巨噬细胞在兔动脉粥样硬化模型斑块中表达的动态变化。方法:24只健康雄性新西兰大耳白兔随机分为试验组(15只)和对照组(9只),试验组在球囊损伤腹主动脉内膜后喂养高脂饮食,对照组喂养普通饲料,于6,12,18周分别处死动物,分离腹主动脉,检测脂质和脂蛋白,应用光学显微镜观察动脉粥样硬化进程,采用免疫组织化学方法分析巨噬细胞在斑块处的表达及定位。结果:高脂饮食喂养后6周,兔动脉内皮受损,12周和18周可见明显动脉粥样硬化斑块形成。与对照组比较,巨噬细胞在动脉粥样硬化斑块处表达增高,主要位于内膜斑块的中下部分;巨噬细胞表达量随着动脉粥样硬化斑块的进展而增多。结论:巨噬细胞的表达随着斑块进展而增多,可能与动脉粥样硬化进展及斑块不稳定相关。 相似文献
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兔颈动脉粥样硬化模型的建立及MR成像的实验研究 总被引:2,自引:1,他引:2
目的建立兔血管内膜损伤性颈动脉粥样硬化模型,并探讨用临床应用型MRI检测动脉粥样硬化的形成过程。方法用动脉球囊介入扩张兔一侧颈总动脉后高脂饲养12周,分别在球囊扩张前及扩张后2、4、8、12周末取外周血检测血脂水平并MRI检查;同时在球囊扩张后12h、6周、12周末取损伤血管进行病理学检查。结果高脂喂养后第2周开始,血脂水平进行性升高;球囊扩张后6周起MRI显示,患侧均出现不同程度的血管壁高信号,12周后,MRI表现为损伤血管壁高信号区增厚并管腔狭窄,对应病理学检查显示:到第6周时,血管平滑肌层增厚,内膜面有少量泡沫细胞形成,血管腔轻度狭窄;12周后,损伤侧颈总动脉明显粥样斑块形成,符合动脉粥样硬化特点。结论用介入动脉球囊扩张损伤加高脂饲养方法可成功建立兔颈动脉粥样硬化狭窄模型,临床应用型MRI可成功检测兔颈动脉粥样硬化的形成过程。 相似文献
3.
环氧化酶-2在动脉粥样硬化中的表达及血清炎性细胞因子的变化 总被引:5,自引:5,他引:5
目的:观察动脉粥样硬化时环氧化酶-2(COX-2)的表达及血清炎性细胞因子6-酮-前列腺素F1α(6-keto-PGF1α)、血栓素B2(TXB2)和肿瘤坏死因子-α(TNF-α)的变化。方法:在高脂兔动脉粥样硬化模型中应用COX-2抑制剂干预,观察粥样硬化斑块形成的病理变化,用单克隆抗体免疫组织化学法观察COX-2在动脉粥样硬化斑块中的表达,并检测各组血脂及血清6-keto-PFG1α、TXB2和TNF-α的变化。结果:高脂饲料组较正常饮食对照组胆固醇(CH)、甘油三酯(TG)、高密度脂蛋白(HDL)及低密度脂蛋白(LDL)血清含量明显增高;两高脂饮食组COX-2在动脉粥样斑块中高度表达,粥样斑块下的平滑肌细胞中有少量表达,对照组动脉无COX-2表达;高脂饲料组(B组)和高脂饲料加美洛昔康组(C组)较对照组(A组)6-keto-PEF1α、TXB2和TNF-α含量明显增高,B组6-keto-PGF1α、TXB2和TNF-α亦较C组含量高。结论:COX-2在动脉粥样斑块中高度表达,并参与动脉粥样硬化病变的炎症过程。COX-2抑制剂可能干预由氧化LDL诱导的前列环素、血栓素及炎症因子的产生。 相似文献
4.
目的探讨不同剂量瑞舒伐他汀对兔颈动脉粥样硬化斑块内的CD147表达水平以及斑块稳定性的影响。方法将40只新西兰雄性大白兔随机分为五组:空白对照组、模型对照组(液氮损伤+高脂饲料建立动脉硬化模型)、低中高浓度药物干预三组(造模后分别予以瑞舒伐他汀1 mg·kg-1·d-1干预、2.5 mg·kg-1·d-1干预和5 mg·kg-1·d-1干预),15周后对兔颈总动脉血管进行病理形态学检查,反转录聚合酶链反应(RT-PCR)检测斑块内CD147 mRNA表达水平及蛋白质印迹法(Western blot)检测斑块内CD147蛋白表达水平。结果第15周末,模型对照组斑块内CD147 mRNA、CD147蛋白表达水平明显高于空白对照组(P<0.05)。病理显示模型对照组颈动脉内可见大量的不稳定斑块,模型对照组的8只兔中5只出现明显斑块破裂及血栓形成,而空白对照组的8只兔血管内膜光滑。瑞舒伐他汀干预,斑块内CD147 mRNA、CD147蛋白表达水平与模型对照组相比明显降低(P<0.05),且具有剂量依赖性,表现为高浓度药物干预组表达水平最低。病理显示瑞舒伐他汀干预后颈动脉动脉硬化斑块均较为稳定,动脉粥样斑块的面积明显减小,斑块纤维帽增厚,且具有剂量依赖性。结论兔颈动脉不稳定斑块内CD147的表达增多;瑞舒伐他汀能通过抑制CD147表达从而发挥其稳定动脉硬化斑块的作用,具有剂量依赖性。 相似文献
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目的:用贵州小香猪建立动脉粥样硬化动物模型,观察小型猪动脉粥样硬化发生发展与血浆C-反应蛋白水平的关系。方法:实验于2003-02/2004-03在南华大学心血管病研究所实验室进行。选择10只贵州小香猪单纯随机分为两组(n=5):①高脂高胆固醇组:喂饲高脂高胆固醇饲料2个月后麻醉状态下切开右侧颈总动脉放置6F动脉球囊导管,压力600~800kPa×180s,重复2次,然后在200~400kPa压力下从远端向近端拖拉球囊导管,并重复3次,术后饲以高脂高胆固醇饲料。②正常对照组:普通饲料喂养2个月后麻醉状态下分离右侧颈总动脉,但不进行血管内膜损伤。实验进行12个月,每2个月检测1次血浆总胆固醇、三酰甘油和高密度脂蛋白胆固醇水平和血浆C-反应蛋白水平,第12个月末处死动物取主动脉和冠状动脉,观察动脉粥样硬化斑块和脂质条纹发生情况。结果:10只小香猪全部进入结果分析。①高脂高胆固醇组小香猪血浆总胆固醇、高密度脂蛋白胆固醇水平从2个月末显著高于正常对照组(P<0.05),而血浆三酰甘油水平从4个月末开始升高,到6个月末才明显增加(P<0.05)。②高脂高胆固醇组小香猪血浆C-反应蛋白水平4个月末时即高于正常对照组(P<0.05),到6个月末明显高于正常对照组(P<0.05)。③在高脂高胆固醇组动物的主动脉、颈总动脉、髂动脉和冠状动脉可见动脉粥样硬化斑块和脂质条纹,该病变区占整个主动脉面积的(90.8±8.3)%;正常对照组未见斑块和脂质条纹。结论:采用血管内膜损伤法加高脂高胆固醇饲料喂养小型猪可建立动脉粥样硬化动物模型。动脉粥样硬化小型猪血浆C-反应蛋白水平升高,C-反应蛋白和动脉粥样化形成相关。 相似文献
6.
纤溶酶原激活物抑制物-1与动脉粥样硬化关系的研究 总被引:3,自引:0,他引:3
目的 通过对动脉粥样硬化(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)表达的研究,探讨PAI-1在AS中的作用.方法 16只雄性大耳白兔随机分为正常饮食组和高脂饮食组,每组8只,饲养16周.两组白兔均于0周、16周取耳缘静脉血,检测血清中PAI-1 的水平;16周后处死,应用免疫组化方法检测PAI-1在主动脉粥样硬化斑块中的表达.结果 正常饮食组和高脂饮食组0周血清中PAI-1水平差异无显著性(P>0.05);高脂饮食组16周后血清PAI-1水平较0周显著增加(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 动脉粥样硬化的发生伴有血清和粥样斑块中PAI-1表达增加,PAI-1可能参与了AS的形成. 相似文献
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目的:观察罗格列酮时兔髂动脉球囊内膜剥脱术后细胞凋亡及凋亡调控蛋白Bcl-2、Bax表达的影响.方法:将30只雄性新西兰大耳白兔随机分为3组,正常对照组(普通饮食)、模型组(高脂饮食+球囊内膜剥脱术)和罗格列酮组(高脂饮食+球囊内膜剥脱术+罗格列酮).分别于术后第1、4周末处死动物,取髂动脉标本行病理形态学观察,TUNEL法检测细胞凋亡水平,免疫组化法测定Bax、Bcl-2蛋白表达的情况.结果:正常对照组仅见少量凋亡细胞和Bax、Bcl-2蛋白表达.与模型组相比,罗格列酮组在术后第1、4周末内膜增殖程度显著减轻(P<0.05),细胞凋亡程度、Bax蛋白表达明显增强(P<0.01),Bcl-2蛋白表达减少(P<0.01),细胞凋亡改变在术后l周末更为明显.结论:罗格列酮具有促进球囊损伤术后内膜平滑肌细胞凋亡、下调Bcl-2蛋白表达及上调Bax蛋白表达的作用. 相似文献
8.
MRI评价兔动脉粥样硬化模型 总被引:1,自引:0,他引:1
马占龙 《中国医学影像技术》2010,26(13):1-3
目的 探讨1.5T MR仪检测兔颈动脉粥样硬化模型中粥样硬化斑块的形成。 方法 用动脉球囊扩张法损伤兔一侧颈总动脉血管内膜后高脂饲养15周,行MRI及损伤血管的病理学检查。 结果 15周后,MRI表现为损伤血管壁高信号区增厚并管腔狭窄,对应病理学检查显示:血管腔狭窄;损伤侧颈总动脉明显粥样斑块形成,符合动脉粥样硬化特点。MR成像与病理学所测血管壁厚度之间有相关关系(r=0.953)。 结论 临床应用型1.5T MRI可成功检测兔颈动脉粥样硬化的形成。 相似文献
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目的:血管内皮生长因子在动脉粥样硬化斑块中的高表达可能会促进斑块的发生与发展。因此,就产生了在动脉粥样硬化进程中局部应用血管内皮生长因子基因治疗心肌缺血是否会产生促进动脉粥样硬化斑块发展的安全性问题。方法:实验于2006-05/2007-03在长海医院胸心外科实验室完成。①实验材料:SPF级雄性新西兰大白兔28只,体质量2.0~2.5kg;表达hVEGF165的腺病毒及表达LacZ的腺病毒AdLacZ由解放军第二军医大学长海医院胸心外科自行构建。②实验分组:将动物随机分为实验组和对照组,每组14只。③实验过程:将28只雄性新西兰大白兔应用球囊损伤 高脂饮食喂养建立动脉粥样硬化模型后平均分成两组:Ad-hVEGF165治疗组和AdLacZ对照组;结扎兔左冠状动脉前降支建立急性心肌缺血模型,载体腺病毒直接心肌内注射治疗。④实验评估:4周、8周后进行兔斑块形态学、病理及心功能检测。结果:①治疗组和对照组兔均形成明显的动脉粥样硬化斑块,苏丹Ⅳ染色为猩红色,两组在斑块面积、斑块周径及斑块最大厚度相比差异无明显统计学意义。②治疗组与对照组心功能在术后4周时相比较术前都有下降,对照组较治疗组下降更明显(P<0.05)。③治疗组心肌毛细血管密度比对照组增加,缺血心肌及动脉粥样斑块中均发现人血管内皮生长因子表达。结论:在应用治疗剂量Ad-hVEGF165治疗心肌缺血时不会促进动脉粥样硬化的发展。 相似文献
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目的采用多种方法制备兔腹主动脉粥样硬化斑块模型,寻求可靠的动脉粥样硬化斑块模型制备方法。方法采用单纯高脂喂养(对照组)、高脂喂养+腹主动脉球囊拉伤术(实验组1)、高脂喂养+注射小牛血清白蛋白(实验组2)、高脂喂养+腹主动脉球囊拉伤术+注射小牛血清白蛋白(实验组3)4种方法建立兔腹主动脉粥样斑块模型,对比评估斑块形成情况。结果实验组腹主动脉内中膜复合体厚度(IMT)均明显高于对照组,实验组与对照组兔腹主动脉粥样斑块回声类型的占比均有显著性差异,实验组粥样斑块形成数目明显多于对照组,其中实验组3的斑块数量较实验组1、实验组2多。结论高脂喂养+腹主动脉球囊拉伤术+注射小牛血清白蛋白是一种稳定、高效的兔腹主动脉粥样硬化斑块模型建立方法,其建模效果优于其他3种方法,是一种稳定、高效的建立斑块模型方法。 相似文献
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多沙唑嗪对兔血脂和血管内膜增生的影响 总被引:1,自引:0,他引:1
目的:探讨多沙唑嗪对兔动脉球囊损伤后血管狭窄的影响及与血脂的关系。方法:23只新西兰兔随机分为3组,正常对照组用普通饲料喂养并不予任何处理。另两组用高脂饲料喂养并行腹主动脉球囊损伤术,多沙唑嗪组术后应用多沙唑嗪控释片4mg/d灌胃,术后4周处死兔,观察各组血脂以及血管损伤处内膜、中膜厚度、新生内膜面积、管腔面积。结果:高脂喂养造成兔血脂明显增高。手术开始时多沙唑嗪组和球囊损伤组两组血脂水平无差异,手术4周后多沙唑嗪组总胆固醇较球囊损伤组降低,而高密度脂蛋白较球囊损伤组增高。术后多沙唑嗪组与球囊损伤组血管损伤处相比血管内膜增生减轻,新生内膜面积减少,管腔面积增加。结论:多沙唑嗪可以抑制高脂喂养加球囊损伤后兔腹主动脉血管的狭窄,可以降低血脂、抑制动脉粥样硬化进展。 相似文献
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目的探讨建立兔动脉粥样硬化模型的方法。方法成年健康新西兰兔10只,随机分为两组,对照组兔常规饲养;模型组兔应用小牛血清清蛋白免疫损伤,高脂饮食喂养,两组均饲养8周。经耳缘静脉取血检测胆固醇、三酰甘油、高密度脂蛋白、低密度脂蛋白及血浆溶血磷脂酸水平;取颈内动脉,应用苏木精-伊红(HE)染色及免疫组化法测定细胞外基质金属蛋白酶诱导因子(Emmprin)和金属蛋白酶组织抑制因子(TIMP-1)表达。结果模型组造模后,血浆溶血磷脂酸水平明显升高,差异有统计学意义(t=11.265,P〈0.05);模型组颈内动脉未形成明显的动脉粥样硬化斑块,Emmprin和TIMP-1未见明显表达。结论免疫损伤-高脂喂养法不易于短期内建立兔动脉粥样硬化模型。 相似文献
13.
背景:近年研究证明,补阳还五汤具有扩张血管、改善微循环、抗炎、抗氧化应激和保护血管内皮细胞的功能,但其具体机制尚不清楚,尤其是对经皮腔内冠状动脉成形后再狭窄形成过程有何影响,目前很少见报道.目的:观察加味补阳还五汤对兔髂动脉球囊损伤后血管狭窄及氧化应激的影响.方法:将新西兰兔以随机抽签法分为对照组、模型组和药物组.对照组给予普通饲料,模型组、药物组给予高脂饮食.饲养2周后,模型组、药物组行髂动脉内膜剥脱术,对照组兔行假手术对照,药物组术后饲料中添加加味补阳还五汤药颗粒2 mL/(kg·d),对照组及模型组喂食同前.4周后光镜观察兔髂动脉内膜的损伤情况,并检测血脂水平、血清超氧化物歧化酶活性和丙二醛水平的变化.结果与结论:对照组髂动脉内膜薄且结构完整,无动脉硬化斑块;模型组内膜增厚,管腔明显狭窄,可见明显动脉粥样硬化斑块;药物组动脉粥样硬化斑块厚度减小,管腔狭窄程度较轻.药物组兔血清总胆固醇、三酰甘油和低密度脂蛋白胆固醇、丙二醛水平明显低于模型组,而高密度脂蛋白胆固醇、血清超氧化物歧化酶水平明显高于模型组(P<0.05).结果说明加味补阳还五汤具有较好的防止家兔球囊扩张损伤髂动脉所致的管腔狭窄及抗实验性动脉粥样硬化作用,其机制可能与其清除氧自由基抗氧化应激、调节脂质代谢等作用有关. 相似文献
14.
Zhang C Yang J Feng J Jennings LK 《The Journal of laboratory and clinical medicine》2002,140(2):119-125
We evaluated the effect of basic fibroblast growth factor (bFGF) on the extent of atherosclerosis and balloon injury-induced vasoproliferation in atherosclerotic animals with acute myocardial infarction (AMI). Fifty-six rabbits were fed a 1% cholesterol diet. Balloon injury of iliac arteries and experimental acute myocardial infarction were induced in the same animals. Rabbits were then randomized to a bFGF group (20 pg/day, intravenously) or a control group (intravenous saline solution). The beneficial effects of bFGF on cardiac function, infarct size, and collateral vessel development, and the possible effect on vasoproliferation of balloon-injured vessels, were measured after 1 and 2 weeks. The extent of atherosclerosis was measured after 1, 2, and 4 weeks. Our results showed that bFGF significantly reduced infarct size and increased collateral-vessel density (P <.01) in infarct areas. Cardiac function was better in the bFGF group than in corresponding controls (P <.05). Similar beneficial effects of bFGF were noted in animals after 1- and 2-week treatments. However, the extent of atherosclerosis and the vasoproliferation in chronic atherosclerotic vessels induced by balloon injury and cholesterol diet were not significantly different between the two groups. Our results suggest that short-term treatment with bFGF enhances collateral development and produces maximum therapeutic benefits without exacerbating atherosclerosis and cell proliferation in stenotic vessels after AMI in atherosclerotic rabbits. 相似文献
15.
目的 研究普罗布考减轻动脉成形术后再狭窄的作用.方法 将30只新西兰大白兔随机分为普罗布考治疗组和对照组各15只.以球囊损伤颈总动脉,用高胆固醇食物饲养8周后切取颈总动脉,HE染色观察血管管腔面积和内膜面积的变化.采用明胶酶谱法和酶法测定动物血清中基质金属蛋白酶2的酶原(pro-MMP-2)、基质金属蛋白酶2(MMP-2)及血清胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)的水平.结果 普罗布考组TC、LDL-C、TG和HDDC水平较对照组低,但差异无显著性(P>0.05);普罗布考组pro-MP-2、MMP-2水平较对照组低,两组比较均具有显著性差异(P<0.05);普罗布考组颈总动脉新生内膜面积、最大内膜厚度明显低于对照组,两者比较差异具有显著性(P<0.05);而普罗布考组颈总动脉管腔面积明显高于对照组后,两者比较差异具有显著性(P<0.05).结论 普罗布考可通过抑制MMPs的途径减轻兔颈总动脉成形术后再狭窄的形成. 相似文献
16.
目的 探讨Batroxobin(DF-521)对动脉粥样硬化兔髂动脉球囊损伤后内膜增生的影响。方法 应用高胆固 醇饮食饲养建立兔髂动脉粥样硬化模型。动物随机分为两组,治疗组(n=10):血管内膜球囊剥脱术后5h静脉推注Batroxobin5^Bu,2.5^Bu隔日1次静注,共6次。对照组(n=8):术前术后不用药。术后30d处死,分离血管,做病理形态学检查和细胞流式测定。结果 ①治疗组损伤血管内膜厚度小于对照组,而管腔模截面积大于对照组(P均<0.01).②治疗组血管壁细胞增殖周期中增殖期细胞数明显低于对照组(P均<0.001)。结论 Batroxobin能抑制动脉粥样硬化髂动脉球囊损伤后血管平滑肌细胞(VSMC)的增殖,减轻内膜增生反应。 相似文献
17.
Ji Qi Shaoqun Zhang Lei Zhang Ruiyue Ping Kaike Ping Da Ye Honggui Shen Yili Chen Yikai Li 《Journal of manipulative and physiological therapeutics》2018,41(2):164-173
Objectives
This study aimed to preliminarily explore the effects of the soft tissue mobilization of pushing on Qiao-Gong (MPQ) on biomechanical properties of the carotid artery using an animal model of carotid atherosclerosis (CAS).Methods
Fifty rabbits were randomly divided into 4 groups: animals with CAS treated with MPQ (CAS-MPQ [n = 15]); animals with CAS treated without MPQ (CAS [n = 15]); normal animals treated with MPQ (normal-MPQ [n = 10]); and a blank control group (n = 10). The MPQ procedure consisted of soft tissue mobilization of the Qiao-Gong acupoint on the front edge of the sternocleidomastoid muscle applied from top to bottom, by flat pushing with the thumb repeatedly for 20 times. Disease in the CAS models was induced by carotid artery balloon injury combined with a high-fat diet for 12 weeks. At the end of modeling, carotid color Doppler ultrasonography examination was performed to confirm which animal models were successfully induced with CAS, excluding model rabbits without typical CAS at the same time. Then, MPQ was applied on rabbits in the CAS-MPQ and the normal-MPQ groups for 3 weeks. By contrast, rabbits in the other 2 groups were fed normally without MPQ. Uniaxial failure tests were later performed on carotid arteries in all 4 groups, and at the end of the study, a 2-way factorial analysis of variance of the results was conducted.Results
(1) At the end of modeling, 10 rabbits in the CAS-MPQ group and 9 in the CAS group were included with typical carotid atherosclerotic characteristics. (2) Young’s elastic modulus of the rabbit carotid artery increased more significantly in the CAS-MPQ group than the CAS group. (3) Compared with normal rabbit carotid arteries, atherosclerotic carotid arteries had lower levels of ultimate stress and ultimate strain but higher levels of ultimate load.Conclusions
The uniaxial tensile mechanical properties of the rabbit atherosclerotic carotid artery were impaired after MPQ. 相似文献18.
Hara M Takeuchi K Fujii Y Maemura E Konishi Y 《Journal of clinical laser medicine & surgery》1991,9(6):453-457
Basic studies were carried out on the treatment, with argon laser and balloon dilatation catheter, of stenotic arteries resulting from atherosclerotic plaque. Seventeen rabbits approximately 34 weeks old and weighing between 3 and 4 Kg were used. Each rabbit was fed a 1% cholesterol diet for 3 to 4 months to induce atherosclerotic lesions in the carotid arteries and the aorta. The argon laser unit used was a Model 20 Endocoagulator (HMG, Inc.; maximum power, 12W). Under an angioscope, two bare-ended laser probes (1.5 mm and 0.3 mm in diameter) were used to vaporize atheromatous plaque in the aortas of 10 rabbits, and a metal tip laser probe in the case of seven rabbits. The plaque remaining after this laser angioplasty was compressed to the luminal surface through inflation of a balloon catheter (balloon angioplasty) in order to sufficiently dilate the arteries. The animals were then sacrificed and examined both macroscopically and microscopically. When the bare-ended probes were used, there was a change in the depth of vaporization in line with the direction of the laser beam. Using a laser heating power of 25 J, perforation of the vessel wall was observed in 36% of the trials. A higher frequency of perforation was seen with the 0.3 mm probe than with the 1.5 mm probe. However, a constant vaporizing effect was achieved using the metal tip laser.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
19.
Zhao SP Wu ZH 《Clinica chimica acta; international journal of clinical chemistry》2005,360(1-2):133-140
BACKGROUND: Leptin may play an important role in the development of atherosclerosis. We evaluated the effect of atorvastatin on leptin secretion in vivo and in vitro. METHODS: Sixteen rabbits fed with high-cholesterol diet for 8 weeks were randomly divided into 2 groups: (1) high cholesterol diet for 6 weeks (n=8), and (2) the same cholesterol diet plus atorvastatin (2.5 mg/kg/day) for 6 weeks (n=8). A control group (n=5) was fed with normal diet for 14 weeks. Subcutaneous adipose was collected for RNA analysis. The direct effect of atorvastatin on leptin release was assayed in primary rabbit adipocytes. Leptin levels in serum and adipocytes culture supernatant were measured by ELISA. RT-PCR was used to evaluate leptin mRNA expressions in adipose and adipocytes. RESULTS: Compared with control group, rabbits fed with high cholesterol diet showed higher levels of serum total cholesterol, LDL cholesterol and leptin, all of which were significantly reduced by atorvastatin treatment. Leptin mRNA expression of adipose was significant lower in rabbits treated with atorvastatin than those fed with high cholesterol diet continuously (0.81+/-0.31 vs. 1.23+/-0.36, P<0.05). Atorvastatin dose-dependently inhibited leptin secretion and mRNA expression in cultured adipocytes. CONCLUSION: Atorvastatin can inhibit leptin release and mRNA expression, and reduces serum leptin level in hypercholesterolemic rabbits. 相似文献