树鼩血清与多种二抗的交叉反应:可在树鼩疾病动物模型中广泛应用

背景:由于树鼩是介于食虫目和灵长目之间的代表,进化程度高,较价廉的灵长类动物,医学生物学的用途很高,已受到广大学者的重视。目的:检测通常用的二抗能否与树鼩的血清发生免疫反应。方法:用Western和ELISA的方法检测树鼩的血清是否与抗兔、抗羊、抗人、抗小鼠、抗大鼠、抗猴的二抗发生交叉反应。结果与结论:Western结果表明树鼩的血清与抗兔、抗羊、抗人、抗小鼠、抗大鼠的二抗均不发生反应,与抗猴的二抗有交叉反应。ELISA的结果也表明树鼩的血清与抗猴的二抗有交叉反应,而与其他二抗没有交叉反应。结果说明通常卖的二抗不能用于树鼩IgG的免疫检测,只有抗猴的二抗与树鼩的血清发生交叉反应,必需制备抗树鼩IgG的单克隆和多克隆抗体,在没有现成抗体可用时,可采用抗猴的二抗替代检测,能在树鼩疾病动物模型的研究中得到广泛应用。     

病毒接种剂量对HBV感染成年树鼩的影响

目的探讨不同病毒接种剂量对乙肝病毒(hepatitis B virus,HBV)感染树鼩进程的影响。方法分别给4组树鼩接种含101、102、104和108GE(genome equivalents)乙肝病毒的感染者血清,于不同时间点采集树鼩血清标本,应用实时荧光定量PCR(real-time fluorescence,PCR)检测血清HBV DNA浓度,用电化学发光免疫测定法(electrochemiluminescence immunoassay,ELICA)检测血清中HBV感染标志物,用临床生化分析仪测定谷丙转氨酶(alanine transaminase,ALT)水平。结果接种108GE HBV后树鼩体内HBV感染持续3周,接种104GE HBV后树鼩体内HBV感染延长至15周,接种101和102GE HBV后树鼩体内HBV感染可以存在9周。结论病毒接种剂量对HBV感染成年树鼩的进程有显著影响,中低剂量(101、102和104GE)接种利于树鼩体内HBV感染的维持。     

树鼩消化道胰高血糖素样肽-1阳性细胞分布的研究

目的观察树鼩胃肠道胰高血糖素样肽-1(GLP-1)免疫反应阳性细胞(EG细胞)分布情况与大鼠消化道的差异,以期为树鼩模型的进一步使用提供参考。方法免疫组化SABC法检测树鼩消化道(口腔、咽除外)GLP-1的细胞阳性含量。结果EG细胞分布于树鼩十二指肠、回肠、结肠、空场中的腺上皮细胞间,阳性物质分布于细胞质。树鼩胃、直肠未见EG细胞分布。回肠免疫组织化学染色结果显示EG细胞阳性,消化道中只有回肠、结肠分布GLP-1阳性较多,树鼩与大鼠相比较消化道中GLP-1差异显著(P0.01)。结论树鼩胃肠道内十二指肠、回肠和结肠、空肠都有胰高血糖素阳性细胞。大鼠只在回肠、结肠有阳性细胞。据GLP-1的作用机理和树鼩消化道GLP-1的分布,树鼩动脉粥样硬化(atherosclerosis,AS)AS模型不易制作可能与GLP-1的作用相关。     

树鼩慢性感染乙肝病毒过程中枯否细胞变化的意义*

 目的：探索枯否细胞在树鼩感染乙肝病毒（HBV）慢性化过程中的意义。方法：树鼩分为3组：A组6只,为前期实验已确定慢性感染HBV的树鼩;B组3只,为疑似慢性感染HBV的树鼩;C组4只,为未接种HBV的正常对照树鼩。全部动物定期抽血和进行肝活检手术;对手术切取的树鼩肝组织进行枯否细胞的分离、纯化和原代培养,采用流式细胞术、细胞免疫组化、溶酶体荧光探针及实时荧光定量RT-PCR等方法检测CD163+细胞数量、溶酶体数量、溶菌酶的表达及肿瘤坏死因子α（TNF-α） mRNA表达水平。结果：（1）慢性感染HBV的树鼩肝脏枯否细胞比例及肝组织内CD163+细胞数量显著高于其它2组（均P<0.05）;（2）慢性感染HBV的树鼩肝脏枯否细胞的溶酶体荧光强度、肝组织内溶菌酶阳性细胞计数和TNF-α mRNA的表达水平均显著低于其它2组（均P<0.05）。结论：枯否细胞在宿主感染HBV的慢性化过程中可能起一定的调节作用。     

过氧化物酶体增殖物激活受体γ对血管平滑肌细胞增殖和动脉粥样硬化形成的影响

目的观察过氧化物酶体增殖物激活受体γ(PPARγ)在动脉粥样硬化形成中的作用,检测其对血管平滑肌细胞(VSMC)增殖的影响,探讨其抗AS的分子机制。方法高脂饮食制作兔动脉粥样硬化模型,石蜡切片HE染色检测AS病变程度。MTT法测定VSMC增殖率,Westernblot检测PPARγ和MMP-9蛋白含量。结果高脂喂养导致兔血清中TC、TG和LDL水平升高,AS斑块形成,吡格列酮可对抗高脂饮食诱导的AS。主动脉粥样斑块中的PPAR-γ蛋白表达较对照组显著增多。吡格列酮可抑制AngⅡ诱导的VSMC增殖,并使高脂喂养的兔主动脉和VSMC中的MMP-9表达减少。结论PPARγ是调节AS的关键分子,被激动剂吡格列酮激活后可能通过下调MMP-9的表达,抑制VSMC的增殖而起到抗AS的作用。     

慢性乙型肝炎病毒感染树鼩Kupffer细胞TLR2和TLR4的表达及其意义

目的探索慢性乙型肝炎病毒(HBV)感染树鼩Kupffer细胞Toll样受体(TLR)家族中的TLR2和TLR4在mRNA水平的表达情况及其对Kupffer细胞功能的影响。方法树鼩分为确定慢性感染HBV的树鼩、疑似慢性感染HBV的树鼩和未接种HBV的正常对照树鼩。全部动物定期抽血和进行肝活检手术,采用实时荧光定量PCR(qRT-PCR)分析血清和肝组织的HBV DNA水平;对手术切取的树鼩肝组织进行Kupffer细胞的分离、纯化和原代培养,采用qRT-PCR检测TLR2、TLR4以及TNF-α的mRNA表达水平;采用迁移实验及溶酶体荧光探针等方法分析TLR2和TLR4对Kupffer细胞迁移能力及溶酶体数量的影响。结果确定慢性感染HBV的树鼩TLR2 mRNA和TLR4 mRNA表达水平均低于疑似慢性感染HBV的树鼩和未接种HBV的正常对照树鼩(P0.05),表达水平均与动物肝组织的HBV DNA拷贝数呈负相关(P0.05),与Kupffer细胞的细胞迁移数、溶酶体密度及TNF-αmRNA表达水平呈正相关(P0.05)。结论 Kupffer细胞中的TLR2和TLR4可能通过影响Kupffer细胞功能而参与树鼩HBV感染后肝脏病变的慢性化发展过程。     

含辛伐他汀药物血清对兔血管平滑肌细胞增殖的直接作用及意义

目的 :探讨辛伐他汀对体外培养兔血管平滑肌细胞增殖的影响及意义。方法 :16只雄性新西兰兔随机分为血清对照组和三个不同剂量的辛伐他汀亚组 (每日分别给予辛伐他汀 5mg/kg、10mg/kg、15mg/kg) ,7天后采血并混合每组 4只兔血 ,无菌分离制备三亚组的辛伐他汀含药血清。采用内皮素 1(ET 1)刺激正常喂饲原代培养兔主动脉血管平滑肌细胞的方法 ,建立血管平滑肌细胞增殖模型。采用MTT及3H TdR法检测各组辛伐他汀含药血清对血管平滑肌细胞增殖的作用。结果 :与不含药的正常对照组相比 ,不同亚组辛伐他汀含药血清呈剂量依赖性抑制血管平滑肌细胞增殖 (P <0 .0 1～0 .0 5 )。结论 :兔口服辛伐他汀后的血清具有抑制血管平滑肌细胞增殖的作用     

川芎嗪对动脉平滑肌细胞形成粥样硬化的影响

目的 :探讨川芎嗪对动脉平滑肌细胞形成粥样硬化的防治机制。方法 :以高脂高胆固醇 (Ｃｈｏ)膳食制备大白兔高脂高Ｃｈｏ血清。贴块培养法进行ＶＳＭＣｓ原代培养及传代。原代培养到第 9～ 12天 ,组织块周围的细胞生长融合成片并铺满瓶底时 ,进行ＶＳＭＣｓ传代培养。实验选用第 3代传代培养的ＶＳＭＣｓ。实验分为正常组用含双抗和胎牛血清的ＲＰＭＩ16 40培养液培养 ,高脂组用含双抗和高脂血清的ＲＰ ＭＩ16 40培养液培养 ,秋水仙碱组用含双抗和高脂血清的ＲＰＭＩ16 40培养液加入秋水仙碱培养 ,川芎嗪低、中、高剂量组用含双抗和高脂血清…     

中药赤芍对球囊损伤术后血管重构的干预研究

目的 观察中药赤芍防止球囊损伤术后血管重构作用。方法 新西兰白兔随机分为对照组、单纯高脂组、赤芍高剂量组、低剂量组。高脂喂养6周建立动脉粥样硬化模型,行颈动脉球囊损伤术,8周时取材作病理形态学检查。结果(1)与高脂组比较,赤芍高、低剂量组增生内膜面积、中层面积,内膜、中膜、外膜PCNA阳性着色均显著减少(P<0.05或P<0.01)。(2)各组内皮增生成分主要为平滑肌细胞;巨噬细胞阳性着色主要分布在外膜,与高脂组比较,赤芍高、低剂量组阳性着色较少。(3)高脂组动脉损伤侧外膜Ⅰ型胶原增多,赤芍组Ⅰ型胶原增加较少。结论 赤芍对高脂喂养兔颈动脉球囊损伤术后血管重构有显著防止作用。     

高脂饲料喂养加静脉注射小牛血清白蛋白建立兔动脉粥样硬化模型**

背景：目前单纯饲喂高脂饲料建立动脉粥样硬化狭窄模型较常见。 目的：采用高脂饲料喂养加静脉注射小牛血清白蛋白建立兔动脉粥样硬化模型。 方法：分别单纯高脂饮食、高脂饲料+脂肪乳灌胃以及高脂饲料+小牛血清白蛋白3种不同的方法喂养兔构建动脉硬化模型,设立正常对照组,予普通饲料喂养。 结果与结论：各组兔血清胆固醇、三酰甘油、低密度脂蛋白和高密度脂蛋白水平较正常对照组显著升高(P < 0.01)。单纯高脂组可出现高脂血症,未发现典型的动脉粥样硬化病变;高脂+脂肪乳灌胃组可形成纤维斑块;高脂+小牛血清白蛋白组可形成较成熟的动脉粥样硬化斑块。结果证实,高脂饲料加静脉注射小牛血清白蛋白可形成较成熟的动脉粥样硬化斑块,可成功建立动脉粥样硬化兔模型。关键词：动脉粥样硬化;小牛血清白蛋白;高脂饲料;兔;动物模型;组织工程 doi:10.3969/j.issn.1673-8225.2012.20.018     

Effect of hyperlipidemic serum and irradiation on wound healing in primary quiescent cultures of vascular cells

After 8 weeks in culture, outgrowths from explants of aortic media of rhesus monkeys and New Zealand rabbits result in circular colonies of mature smooth muscle cells, quiescent in 10% serum. Such cultures were wounded by cutting out a 1.5-mm-wide strip. Migration of cells into the wound area was measured daily, and proliferation was assessed by [3H]thymidine incorporation. Migration began within 24 hr and at 7 days the defect was filled by proliferates of migrated cells. The cumulative labeling index was highest in the cells in the wound gap but was also increased in the remaining part of the culture. Wounding thus stimulated the uninjured portion of these primary cultures to proliferate, while in subcultures of these cells increase in [3H]thymidine incorporation was confined to the wound area. While hyperlipidemic serum has been shown to induce proliferation in unwounded cultures, it did not enhance cell replication elicited by wounding but reduced cell density and labeling index in the wound gap. Irradiation prior to wounding reduced cell proliferation to control values, while migration of cells was not significantly affected. In irradiated cultures, the inhibitory action of hyperlipidemic serum on cell migration became evident. Such quiescent cultures thus allow us to separate the effects of a specific injury on the proliferative and migratory responses of vascular smooth muscle.     

Genistein supplementation inhibits atherosclerosis with stabilization of the lesions in hypercholesterolemic rabbits

The effect of genistein on aortic atherosclerosis was studied by immunohistochemistry with RAM-11 and HHF-35 antibodies and western blotting for matrix metalloproteinase-3 (MMP-3) in New Zealand White rabbits. After provocation of atherosclerosis with hyperlipidemic diet, the rabbits were divided as hyperlipidemic diet group (HD), normal diet group (ND) and hyperlipidemic plus genistein diet group (HD+genistein) for 4 and half months. The average cross sectional area of atherosclerotic lesion was 0.269 mm2 after provocation. The lesion was progressed by continuous hyperlipidemic diet (10.06 mm2) but was increased mildly by genistein (0.997 mm2), and decreased by normal diet (0.228 mm2). The ratio of macrophages to smooth muscle cells in the lesion was not changed by genistein supplementation. The western blotting showed reduction of MMP-3 expression in HD+genistein and ND groups than HD group. The inhibition of atherogenesis by genistein was might be due to improve the endothelial dysfunction rather than direct action on macrophages and/or smooth muscle cells in the lesion, since endothelial dysfunction by lipid peroxidation was the main atherogenic factor in the hypercholesterolemic rabbits. The genistein supplementation also suggests that it helps the stabilization of the atherosclerotic lesion by inhibition of MMP-3 expression.     

Experimental obstructive coronary atherosclerosis in the hyperlipidemic hamster

The evolution of coronary atherosclerotic lesions induced by a hyperlipidemic diet was examined in male hamsters subjected for up to 40 weeks to a standard chow supplemented with 3% cholesterol and 15% butter. Control animals were fed standard chow only. Five to seven hamsters were monthly sacrificed and investigated for serum lipids and coronary artery lesions. As compared with control animals, the hamsters fed the fat diet showed a progressive increase in serum cholesterol which reached maximum values up to 17 fold in the 10th month. The serum of the hyperlipidemic hamster examined by agarose electrophoresis, Laurell immunoelectrophoresis and cross-immunoelectrophoresis showed at most a 14 fold increase in low density lipoproteins after 10 months diet. The examination of coronary arteries revealed morphologic changes already detectable at 2 weeks of diet. The earliest modifications observed were characterized by proliferation of the subendothelial matrix or/and the appearance of liposome-like structures in the intima. After 2-3 weeks of diet, smooth muscle cells appeared occasionally in the intima and monocytes adhered and penetrated through the endothelium. Later on, smooth muscle cells and macrophage displayed lipid deposits. Focally, in areas of intimal proliferation and foam cells, endothelial cells were also lipid-loaded. Like in human atherosclerotic plaque, in the late stages of hamster coronary lesions, there was a progressive accumulation of extracellular unesterified cholesterol, calcium deposition and necrosis. Lesions evolved to a progressive narrowing of the coronary branches affected, with complete obstruction of some small arterial ramifications. Hamster appears to be a suitable model for studying the molecular and cellular events leading to obstructive coronary atherosclerosis.     

细胞外基质及其筑构对平滑肌细胞增殖的影响

目的:研究细胞外基质层粘连蛋白(Laminin,LN),纤维连接蛋白(Fibronecfin,FN)和三维基膜基质Matrigel胶对平滑肌细胞增殖的作用。方法:将用酶消化法分离的兔主动脉平滑肌细胞种植在LN和FN上及三维基膜基质Matrigel胶里,然后用Brdu法检测各平滑肌细胞的增殖率。结果:生长在FN上的平滑肌细胞增殖率最高(24%),生长在LN上的平滑肌细胞增殖率次之(17%),而生长在三维基膜基质胶里的平滑肌细胞未出现细胞增殖,另外LN较FN有明显的促进平滑肌细胞分化成熟的作用。结论:细胞外基质成分和基质筑构对平滑肌细胞的增殖与分化具有重要的调节作用。     

Antiatheromatous properties of elastase in cholesterol-fed rabbits and ex vivo suppressive effect of elastase on smooth muscle cell proliferation in the presence of hypercholesterolemia

The effects of a clinical oral dose of elastase on aortic atheroma development were studied in 0.2% cholesterol-fed rabbits, with or without endothelial denudation, using a balloon catheter. Elastase slightly decreased the serum lipids, but there was no significant difference from the serum lipids in the control groups. However, elastase significantly reduced the surface involvement of Sudan IV-positive staining areas of the aortas in rabbits with and without endothelial injury. The effect of elastase on SMC proliferation stimulated by hypercholesterolemia (C-serum or C-plasma) was also investigated in ex vivo experiments. The cholesterol levels in the serum and plasma of the elastase group were not significantly different from those of the 0.5% cholesterol-fed control rabbits. Proliferation of aortic smooth muscle cells was stimulated in the control group, while such stimulation in the elastase group was significantly lower. Therefore, elastase may suppress the stimulation through plasma factors, hence a reduction in atheroma development would ensue.     

Population dynamics of arterial cells during atherogenesis. VIII. Separation of the roles of injury and growth stimulation in early aortic atherogenesis in swine originating in pre-existing intimal smooth muscle cell masses.

This is a study of focal masses of smooth muscle cells that are found normally in the intima of large and medium sized arteries from intrauterine life to old age in man and most experimental animals. These intimal cellular masses are of special interest because they appear to be sites of predilection for atherogenesis.The experimental animals used in this study were young swine; intimal cellular masses were those in the abdominal aorta; arterial cell population changes were studied from approximately the 8th to the 16th weeks of life and comparisons were made between normolipidemic and hyperlipidemic swine; methods included overall cell counts and isotopic techniques designed to trace cells through multiple divisions. Fifteen swine were given [³H]thymidine on approximately the 60th day of life. Five were sacrificed on the 75th day as a baseline group; five were fed a hyperlipidemic diet from the 75th to the 135th day of life and the remaining five were continued on a conventional low-cholesterol mash diet until the 135th day, when both groups were sacrificed. Total smooth muscle cells in intimal cellular masses of the abdominal aorta averaged 1.59 million in the 75-day-old baseline group; 2.06 million in the 135-day-old mash-fed group; and 4.73 million in the 135-day-old hyperlipidemic group. This tripling in the number of cells in intimal cellular masses of hyperlipidemic swine (as compared to no significant increase in the corresponding value in mash-fed swine) during the initial 60 days on the diet occurred prior to development of overt gross lesions and probably represents the earliest phase of atherogenesis. In the isotopic portion of the study, we attempted to trace the behavior of the original cell population of the intimal cellular masses (re smooth muscle cell births and deaths) for the 60 days in the two dietary groups and to identify differences that accounted for the 2- to 3-fold greater increase of cells in the hyperlipidemic diet group. In regard to cell loss (probably by death) in the mash-fed group, 39% of the cells present at the onset were lost (without surviving progeny) over the 60 days as compared with 40% in the hyperlipidemic group—hence no significant difference.In regard to percentage of original cells surviving but not dividing in 60 days in the mash-fed group, the value was 30% and in the hyperlipidemic no non-dividers were detected; thus more cells were recruited from non-dividers into the active dividing population in the hyperlipidemic group. As regards the 60-day dividing population in the mash dict group, 31% of the original cells divided one or more times with an average of 3.66 live progeny per dividing cell; in the hyperlipidemic group 60% divided one or more times with an average of 5.27 live progeny per divided cell. Thus, the hyperlipidemic diet produced a mitogenic effect on the smooth muscle cells of the intimal cellular masses manifested by significantly larger numbers of cells in the 60-day dividing population and by significantly more divisions per dividing cell (and hence more progeny) than in the mash-fed group. Smooth muscle cell losses were negligible in the media of both groups; numbers of cells were increased considerably in both by growth as expected and no differences were observed in this respect between the two groups.The cell losses in the intimal cellular masses, though apparently not related to the diet at this stage of atherogenesis, probably accounted for localization of the diet-related changes to the intimal cellular masses in the hyperlipidemic swine.     

ANTIATHEROMATOUS PROPERTIES OF ELASTASE IN CHOLESTEROL-FED RABBITS and EX VIVO SUPPRESSIVE EFFECT OF ELASTASE ON SMOOTH MUSCLE CELL PROLIFERATION IN THE PRESENCE OF HYPERCHOLESTEROLEMIA

The effects of a clinical oral dose of elastase on aortic atheroma development were studied in 0.2% cholesterol-fed rabbits, with or without endothelial denudation, using a balloon catheter. Elastase slightly decreased the serum lipids, but there was no significant difference from the serum lipids in the control groups. However, elastase significantly reduced the surface involvement of Sudan IV-positive staining areas of the aortas in rabbits with and without endothelial injury. The effect of elastase on SMC proliferation stimulated by hypercholesterolemia (C-serum or G-plasma) was also investigated in ex vivo experiments. The cholesterol levels in the serum and plasma of the elastase group were not significantly different from those of the 0.5% cholesterol-fed control rabbits. Proliferation of aortic smooth muscle cells was stimulated in the control group, while such stimulation in the elastase group was significantly lower. Therefore, elastase may suppress the stimulation through plasma factors, hence a reduction in atheroma development would ensue.     

Sequential change of DNA synthesis in cultured aortic smooth muscle cells stimulated by hyperlipidemic serum

Smooth muscle cells from monkey aorta quiescent in 5% calf serum have been shown to be stimulated to renewed proliferation by hyperlipidemic serum or LDL from such serum. This proliferative response evidently is not dependent on platelet-derived growth factor present in our system in large quantities. The least exposure time required for reaction between the mitogen and the cells in order to initiate maximal DNA synthesis by this mechanism was studied using autoradiography. Stationary primary cultures and subcultures from monkey aortic media required at least 4 and 8 hr of contact with hyperlipidemic serum or LDL so that a significant number of cells reentered the mitotic cycle. Compared to the primary culture system, subcultures needed a slightly longer time of contact with serum to initiate DNA synthesis. Since there was no significant difference in labeling index between the primary cultures stimulated by serum for 8 and 48 hr and the subcultures exposed between 6 and 48 hr, it is concluded that a relatively brief stimulation commits the majority of responsive cells to reenter the cycle and initiate DNA synthesis.     

Model system to study interaction of platelets with damaged arterial wall. II. Inhibition of smooth muscle cell proliferation by dipyridamole and AH-P719

A new in vivo model for the initial events in atherogenesis was employed to investigate drugs which may inhibit intimal muscle cell proliferation following repeated limited endothelial cell injury. An artery forceps was placed over the central artery of the ear of an anesthetized rabbit for 30 min. The forceps were removed, blood flow resumed in the vessel, and platelets contacted the damaged vessel wall. When a vessel was injured two or more times the smooth muscle cells of the media migrated into the intima and proliferated there between 1 and 3 weeks after the last injury despite restoration of an apparently intact endothelium. The intima of control undamaged vessels sometimes contained a few individual smooth muscle cells while vessels injured two, four, or six times showed correspondingly increasing numbers of layers of intimal smooth muscle cells covering increasing amounts of the intima. Arteries from thrombocytopenic rabbits showed, at most, a single layer of smooth muscle cells covering a small area. In rabbits pretreated with dipyridamole (1.5 mg/kg) for 3 days before each injury, proliferation was also limited to a small area. Neither aspirin (8 mg/kg) nor ticlopidine (40 mg/kg, 5X over 3 days), which inhibit platelet aggregation ex vivo, nor the continuous presence of heparin (800 U/kg, bid), reported to inhibit smooth muscle cell growth in vitro and in vivo, prevented smooth muscle cell proliferation in response to two injuries. However, a potent inhibitor of platelet cyclic-adenosine monophosphate (cAMP) phosphodiesterase, AH-P719 (1.5 or 2.1 mg/kg), was able to inhibit intimal smooth muscle cell proliferation in doses that inhibited platelet aggregation ex vivo.     

动脉粥样硬化模型兔血管平滑肌细胞增殖与癫狂梦醒汤的干预

背景：现代临床研究表明癫狂梦醒汤能够治疗神经官能症、更年期综合征、癔病、老年痴呆等精神系统疾病。 目的：观察癫狂梦醒汤对动脉粥样硬化模型兔血管平滑肌细胞增殖的影响。 方法：将32只日本大耳白兔随机分成空白对照组、模型组、癫狂梦醒汤组、辛伐他汀组,分别给予普通饲料、高脂饲料、高脂饲料+癫狂梦醒汤、高脂饲料+辛伐他汀进行干预,喂养至第12周末。 结果与结论：喂养高脂饲料成功建立动脉粥样硬化模型,模型组有严重的动脉粥样硬化病理改变,增殖细胞核抗原、血小板源生长因子B蛋白表达明显升高,平滑肌细胞呈合成型改变;癫狂梦醒汤组及辛伐他汀组动脉粥样硬化病变明显减轻,增殖细胞核抗原、血小板源生长因子B蛋白表达明显下降(P < 0.01),平滑肌细胞接近“收缩型”改变。结果可见癫狂梦醒汤可抑制血管平滑肌细胞增殖,延缓动脉粥样硬化发生发展,这一作用可能是通过抑制增殖细胞核抗原、血小板源生长因子B蛋白表达来实现的。