十两茶提取物抗高脂诱导家兔动脉粥样硬化形成涉及调节ADMA/NO通路

目的：观察十两茶提取物对高脂诱导家兔动脉粥样硬化的影响。方法：家兔高脂饲料喂养4周后,分别灌胃给予不同剂量的十两茶提取物（25、50和100mg/kg）,共4周。实验结束后,颈动脉取血检测红细胞变形能力,测定血脂、NO、非对称二甲基精氨酸（ADMA）和丙二醛（MDA）含量;分离胸主动脉检测脂质斑块面积和血管内皮依赖性舒张功能。结果：十两茶提取物能剂量依赖性地降低高脂饲养家兔血清总胆固醇和低密度脂蛋白水平,同时显著减少主动脉粥样斑块面积和改善血管内皮舒张功能及红细胞变形能力。十两茶提取物显著降低血清MDA和ADMA含量和增加NO水平,且呈剂量依赖性。结论：十两茶提取物具有抗动脉粥样硬化作用,其机制与抑制脂质过氧化、调节ADMA/NO系统,改善血管内皮功能和红细胞变形能力有关。     

瓜蒌皮提取物对大鼠血管内皮损伤的保护作用

目的研究瓜蒌皮提取物（EPT）对低密度脂蛋白（LDL）诱导的血管内皮损伤的保护作用。方法 48只SD大鼠在乙醚麻醉下,舌下静脉注射人血清LDL（4mg/kg）诱发血管内皮功能损伤。检测血中非对称性二甲基精氨酸（ADMA）、丙二醛（MDA）、一氧化氮（NO）和肿瘤坏死因子-α（TNF-α）的含量。结果单次静注LDL（4mg/kg）显著增加血液中ADMA、MDA和TNF-α水平,降低血液中NO水平。用水和70%乙醇洗脱的瓜蒌皮提取物能显著抑制ADMA、MDA和TNF-α浓度升高及增加血液中NO水平。结论瓜蒌皮提取物对LDL诱导的血管内皮细胞损伤有保护作用,其保护作用与降低ADMA浓度有关。     

高胆固醇血症家兔NO合成酶抑制物含量与脂质过氧化的关系(英文)

目的:探讨高脂饲养家兔血中NO合成酶抑制物二甲基精氨酸(DMA)含量变化与脂质过氧化的关系。方法:检测高脂饲养家兔血清总胆固醇、甘油三脂、丙二醛(MDA)及DMA含量,并观察离体胸主动脉内皮依赖性舒张反应。结果:高脂饲养家兔血脂、血清MDA和DMA含量比正常组增加(MDA为2.88±s0.20vs1.54±0.13nmol·L~(-1),P<0.01,DMA为1.51±0.07vs0.75±0.13μmol·L~(-1),P<0.01),胸主动脉舒张反应降低(最大舒张％为45.59±3.1vs76.93±5.68％)。维生素E抑制MDA升高的同时降低DMA含量及改善内皮舒张功能。结论:高脂血症家兔血清DMA含量的升高可能与脂质过氧化的增加有关。     

Cariporide对糖基化终末产物所致血管内皮损伤的保护作用

目的观察选择性Na /H 交换蛋白1(NHE-1)抑制剂Cariporide对外源性糖基化终末产物(AGEs)所致大鼠血管内皮功能损伤的保护作用。方法将体外制备的糖基化牛血清白蛋白(AGEs-BSA)通过尾静脉注射的方法,1次.d-1,连续4周,诱导大鼠血管功能损伤,治疗组同时给予Cariporide(0.1、1 mg.kg-1.d-1)灌胃。4周后处死动物,取胸主动脉用于血管内皮依赖性舒张功能的检测,主动脉弓做NF-κB-p65免疫组化检测,并测定血清NO及MDA含量。结果大鼠注射AGEs-BSA后,主动脉对乙酰胆碱诱导的内皮依赖性舒张反应明显降低,大鼠血清MDA水平增加,NO水平降低;Cariporide呈剂量依赖性改善AGEs-BSA所致大鼠胸主动脉内皮依赖性舒张反应降低,抑制AGEs-BSA引起的血清MDA浓度升高和血清NO的减少;给予AGEs-BSA后大鼠血管内皮NF-κB活性明显增加,Cariporide能明显抑制AGEs-BSA诱导的NF-κB活化。结论Cariporide对外源性AGEs诱导的大鼠血管内皮功能损伤具有保护作用,其保护作用可能与降低氧化应激、抑制血管内皮细胞的NF-κB活化有关。     

高胆固醇血症改变大鼠血管功能及动脉平滑肌细胞钾通道基因表达(英文)

目的:研究高胆固醇血症对大鼠主动脉功能及主动脉平滑肌上内向整流和ATP敏感钾通道基因表达的影响。方法:大鼠灌胃高胆固醇乳剂两周,制备带内皮和去内皮的主动脉血管环检测收缩和舒张反应,应用RT-PCR观察基因表达的变化。结果:高胆固醇血症明显损伤血管内皮功能,但不影响血管内皮非依赖性舒张反应;在高胆固醇血症血管平滑肌中Kir6.2mRNA表达明显升高(P<0.05),而Kir3.1mRNA表达却显著降低(P<0.05)。结论:高胆固醇血症可改变血管功能,并影响某些内向整流和ATP敏感钾通道亚型的基因表达。     

卡托普利对蛋氨酸所致血管内皮功能损伤的保护作用与对氧磷酶1的关系

目的探讨卡托普利对高蛋氨酸饮食所致大鼠血管内皮功能损伤的保护作用及其机制。方法将蛋氨酸通过灌胃的方法,1次.d-1,连续4周,诱导大鼠血管功能损伤,治疗组同时给予卡托普利、依那普利、N-乙酰半胱氨酸灌胃。4周后处死动物,检测血清一氧化氮(nitric oxide,NO)、丙二醛(malondialdehyde,MDA)含量、对氧磷酶(paraoxonase 1,PON1)、超氧化物歧化酶(superoxide dismutase enzyme,SOD)、血管紧张素转换酶(an-giotensin-converting enzyme,ACE)活性。取胸主动脉检测由乙酰胆碱(acetylcysteine,Ach)诱导的血管内皮依赖性舒张反应。结果高蛋氨酸损伤组大鼠血管内皮依赖性舒张反应显著减弱,血清中MDA浓度升高,PON1活性、血浆NO浓度与SOD活性降低;卡托普利、N-乙酰半胱氨酸和依那普利能显著改善血管内皮依赖性舒张反应、降低MDA浓度、提高血清中的PON1活性、SOD活性和NO浓度。结论卡托普利能够改善高蛋氨酸引起的血管内皮功能的损伤,该作用可能与保护PON1活性及其抗氧化作用、促进内皮细胞释放NO有关。     

高脂血症患者AngⅡ和NO与IGF-1关系研究及通心络疗效

目的研究临床高胆固醇血症患者血管紧张素Ⅱ(AngⅡ)和一氧化氮(NO)与胰岛素样生长因子(IGF-1)相关性,探讨通心络干预疗效。方法观察入选的40名高胆固醇血症患者(TC>5.72mmol·L-1或LDL-C>3.64mmol·L-1)和35名健康体检者血管内皮依赖性舒张功能,并检测血清中AngⅡ、NO、IGF-1和可溶性E-选择素含量的变化,对高胆固醇血症患者AngⅡ与IGF-1以及NO与IGF-1进行pearson相关分析,并将40例高胆固醇血症患者,随机双盲分成两组,通心络组:20例,在常规饮食控制基础上,予通心络胶囊每次4粒(每粒为0.26g),每日3次,安慰剂组:20例,在常规饮食控制基础上服用安慰剂,疗程为8wk,观察通心络对上述指标以及血脂的影响。结果与健康体检者相比,高胆固醇血症患者血清NO和IGF-1含量明显降低,血管内皮依赖性舒张功能下降,而AngⅡ、可溶性E-选择素含量明显增高。高胆固醇血症患者AngⅡ与IGF-1呈负相关(r=-0.406,P<0.01),NO与IGF-1呈正相关(r=0.718,P<0.001)。使用通心络治疗8wk后,IGF-1、NO明显增加,血管内皮依赖性舒张功能明显改善,AngⅡ和可溶性E-选择素降低。结论IGF-1含量降低可能是高胆固醇血症患者血管内皮功能障碍的一个重要机制,通心络提高IGF-1水平可能是其对高胆固醇血症患者血管内皮保护的新机制。     

糖尿病大鼠内源性ADMA升高与代谢控制的关系

目的　以链脲佐菌素诱导的糖尿病大鼠为实验模型 ,研究内源性一氧化氮合酶 (NOS)抑制物非对称性二甲基精氨酸 (ADMA)升高与糖尿病代谢控制的关系。方法　用高效液相色谱测定大鼠血清ADMA浓度 ;用离体胸主动脉环检测乙酰胆碱诱导的内皮依赖性舒张反应 ;并检测血糖、糖基化血清蛋白和血清脂质过氧化产物丙二醛 (MDA)浓度以反映代谢控制。结果　糖尿病大鼠血清ADMA浓度比正常组大鼠明显升高 ,并伴有离体血管内皮依赖性舒张反应的显著抑制 ;经胰岛素治疗 8wk后 ,不仅阻止内源性ADMA的升高 ,也明显改善血管的内皮依赖性舒张功能。此外 ,糖尿病大鼠血糖、糖基化血清蛋白和血清MDA水平也比正常组明显升高。用胰岛素改善代谢控制后 ,血糖、糖基化血清蛋白和血清MDA水平均恢复正常 ,血中ADMA浓度也显著降低。结论　糖尿病大鼠血中内源性NOS抑制物ADMA浓度升高与代谢控制密切相关 ;胰岛素逆转糖尿病大鼠内源性ADMA升高可能与纠正代谢紊乱和降低脂质过氧化有关     

芝麻素对2型糖尿病大鼠主动脉内皮功能的保护作用

目的探讨芝麻素改善2型糖尿病大鼠主动脉内皮功能损伤的作用及可能机制。方法采用长期高脂饮食加小剂量链脲佐菌素(streptozotocin,STZ)建立2型糖尿病大鼠模型。灌服不同剂量芝麻素(120、60 mg.kg-1.d-1)8周后处死动物。离体血管灌流法测大鼠主动脉内皮依赖性舒张反应及NO生物活性,测血清丙二醛(malondialdehyde,MDA)含量和总抗氧化能力(total antioxidative capacity,T-AOC),Western blot测主动脉内皮型一氧化氮合酶(endothelial nitricoxide synthase,eNOS)、硝基酪氨酸(nitrotyrosine,NT)和还原型辅酶Ⅱ(NADPH)氧化酶亚基P47phox蛋白表达。结果与模型组相比,芝麻素(120 mg.kg-1.d-1)组内皮依赖性血管舒张功能增强,NO活性升高;血清MDA含量降低,T-AOC水平升高;主动脉eNOS蛋白表达增高,NT和P47phox蛋白表达降低。结论芝麻素可改善糖尿病大鼠血管内皮功能,其机制与上调血管eNOS表达和减轻NO氧化失活有关。     

丙丁酚对冠心病血管内皮功能的影响

目的观察丙丁酚（普罗布考）对冠心病血管内皮功能的影响。方法采用高分辨率超声诊断系统检测35例确诊冠心病的老年患者服用普罗布考前后肱动脉血流介导的舒张功能（即内度依赖性舒张功能，FMD）和硝酸甘油介导的舒张功能（非内皮依赖性舒张功能，NMD）的变化，同时检测治疗前后血浆一氧化氮（NO）、内皮素（ET）水平的变化，并与28例未接受调脂治疗的老年冠心病患者进行对照研究。结果接受普罗布考治疗的患者ET、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）水平明显降低，而NO和FMD明显增加，NMD无显著性改变。结论普罗布考在降脂的同时能够改善老年冠心病患者血管内皮功能，且该作用独立于高密度脂蛋白胆固醇（HDL-C）水平的降低。     

Probucol preserves endothelial function by reduction of the endogenous nitric oxide synthase inhibitor level

1. Oxide low-density lipoprotein (ox-LDL) is believed to play an important role in early events of atherogenesis, and asymmetric dimethylarginine (ADMA) is associated with the development of endothelial dysfunction. The present study examined the effect of a single injection of native low-density lipoprotein (LDL) on endothelium function and the serum level of ADMA and the effect of probucol on endothelium function and ADMA level in rats. 2. Endothelial injury was induced by intravenous injection of LDL at the dose of 2, 4, or 6 mg kg(-1) for 24, 48, or 72 h, and vasodilator responses to acetylcholine in the aortic rings and serum levels of ADMA, nitrite/nitrate (NO) and malondialdehyde (MDA) were determined. 3. Pretreatment with LDL markedly reduced endothelium-dependent relaxation in a concentration-dependent manner. Inhibition of vasodilator responses to acetylcholine by LDL was abolished in the presence of L-arginine (3 x 10(-4) M). Serum levels of ADMA and MDA were significantly elevated in the rats pretreated with LDL, while serum level of nitrite/nitrate was markedly decreased. 4. Pretreatment with probucol significantly improved endothelium-dependent relaxation, decreased concentrations of ADMA and MDA and increased nitrite/nitrate level in the rats treated with LDL. A similar effect was seen in the rats pretreated with an antioxidant vitamin E. 5. These results suggest that a single injection of native LDL causes endothelial dysfunction by elevation of ADMA levels and that the protective effect of probucol on endothelial cells is related to reduction of ADMA concentration.     

Taurine protects against low-density lipoprotein-induced endothelial dysfunction by the DDAH/ADMA pathway

Asymmetric dimethylarginine (ADMA), a major endogenous nitric oxide (NO) synthase inhibitor, is thought to be a key contributor for endothelial dysfunction. Decrease in activity of dimethylarginine dimethylaminohydrolase (DDAH), a major hydrolase of ADMA, causes accumulation of ADMA in some risk factors of atherosclerosis, including hypercholesterolemia. Taurine is a semi-essential amino acid that has previously been shown to have endothelial protective effects. The present study was to test whether the protective effect of taurine on endothelial function is related to modulation of the DDAH/ADMA pathway. A single injection of native LDL (4 mg/kg, i.v.) markedly reduced endothelium-dependent vasorelaxation and the plasma level of NO, and increased plasma concentrations of ADMA, malondialdehyde (MDA) and tumor necrosis factor-alpha (TNF-alpha). Treatment with taurine in vivo (60 or 180 mg/kg) significantly attenuated the inhibition of endothelium-dependent vasorelaxation and the reduced level of NO, and decreased the elevated levels of ADMA, MDA, and TNF-alpha. Incubation human umbilical vein endothelial cells (HUVECs) with ox-LDL (100 microg/ml) for 24 h markedly increased the medium levels of lactate dehydrogenase (LDH), ADMA, TNF-alpha and MDA, and decreased the level of NO in the medium and the intracellular activity of DDAH. Taurine (1 or 5 microg/ml) significantly attenuated the increases in the levels of LDH, ADMA, TNF-alpha and MDA, and the decrease in the level of NO and the activity of DDAH induced by ox-LDL in HUVECs. The present results suggested that taurine protected against endothelial dysfunction induced by native LDL in vivo or by ox-LDL in endothelial cells, and the protective effect of taurine on the endothelium is related to decrease in ADMA level by increasing of DDAH activity.     

A reduction of endogenous asymmetric dimethylarginine contributes to the effect of captopril on endothelial dysfunction induced by homocysteine in rats

We examined whether captopril exerts beneficial effect on homocysteine-induced endothelial dysfunction in vivo and whether this effect of captopril is associated with a reduction of endogenous inhibitor of nitric oxide synthase (NOS) asymmetric dimethylarginine (ADMA) in rats. Male Sprague-Dawley rats were given intravenous injections of homocysteine (10 mg/kg/day) to induce endothelial dysfunction. Captopril treatment (3 mg/kg/day, i.v.) was taken in some rats after homocysteine administration. Endothelium-dependent relaxation was tested in aortic rings. Serum levels of ADMA, nitrite/nitrate, malondialdehyde (MDA), and creatinine were measured. Furthermore, superoxide dismutase activity in liver and angiotensin converting enzyme activity in serum were also assayed. Administration of homocysteine to rats for 4 weeks significantly impaired endothelium-dependent relaxation compared with control rats. This impairment of endothelium-dependent relaxation was accompanied by elevated serum concentration of ADMA and decreased serum content of nitrite/nitrate. Moreover, serum concentration of MDA was remarkably increased, whereas liver superoxide dismutase activity was decreased in homocysteine-treated group compared with control. Chronic captopril treatment not only improved the impaired endothelium-dependent relaxation, but also prevented the elevation of serum ADMA and MDA levels, as well as reduction of serum nitrite/nitrate contents and liver superoxide dismutase activity. Serum angiotensin converting enzyme activity and creatinine had no significant difference between the three groups. These results suggest that chronic captopril treatment reduces endogenous inhibitor of NOS in rats with homocysteine injection, which may contribute to the beneficial effect of captopril on homocysteine-induced endothelial dysfunction in vivo, and may be secondary to the antioxidative action of captopril.     

Effect of fenofibrate on LDL-induced endothelial dysfunction in rats

Previous investigations have demonstrated that asymmetric dimethylarginine (ADMA) is an important factor contributing to endothelial dysfunction, and that fenofibrate has a protective effect on the endothelium in hyperlipidaemic patients. In the present study in rats treated with native low-density lipoprotein (nLDL), we addressed the question of whether the beneficial effect of fenofibrate on endothelial cells is related to reduction of the ADMA concentration. A single injection of nLDL (4 mg/kg, 48 h) markedly reduced endothelium-dependent relaxation in response to acetylcholine and the plasma level of nitrite/nitrate and increased the plasma concentrations of ADMA, malonyldialdehyde (MDA) and tumour necrosis factor- (TNF-). Treatment with fenofibrate (30 or 100 mg/kg) significantly reduced the inhibition of vasodilator responses to acetylcholine, decreased the elevated levels of ADMA, MDA and TNF-, and enhanced the decreased level of nitrite/nitrate in the rats treated with LDL. These results suggest that the protective effect of fenofibrate on endothelial cells in rats treated with LDL may be related to the reduction of ADMA concentration.     

苦丁茶对高胆固醇脂血症小鼠血清多不饱和溶血磷脂酰胆碱的改善作用

目的:研究苦丁茶水提取物对高胆固醇脂血症小鼠血清中多不饱和溶血磷脂酰胆碱的改善作用。方法:采用LCQTOF-MS/MS和LC-QTRAP-MS/MS建立小鼠血清中多不饱和溶血磷脂的液质联用定性和定量分析方法;采用高脂饲料喂养30 d诱发小鼠高胆固醇脂血症模型;以5,10,15 g·kg^-1·d^-1(按生药材量计算)苦丁茶水提取物连续灌胃给药4周,观察高胆固醇脂血症小鼠血清总胆固醇、低密度脂蛋白胆固醇的变化;观察小鼠肝脏油红O染色后的病理切片;同时,利用上述建立的液-质联用分析方法检测给药后小鼠血清中多不饱和溶血磷脂酰胆碱相对含量的变化。结果:苦丁茶水提取物能够显著降低由高脂饲料诱发的胆固醇脂血症小鼠血清总胆固醇、低密度脂蛋白胆固醇;对小鼠肝脏的脂肪堆积具有明细的抑制作用;同时,与正常小鼠相比,模型小鼠血清中的多不饱和溶血磷脂酰胆碱的相对含量显著下降,而苦丁茶水提取物对该类脂质成分具有显著的回调作用。结论:苦丁茶水提取物对高胆固醇脂血症小鼠血清中多不饱和溶血磷脂的回调作用可能涉及苦丁茶降血脂的药效作用机制,值得深入研究。     

白藜芦醇对高脂血症大鼠血小板聚集的影响及其机制研究

目的:研究白藜芦醇对高脂血症大鼠血小板聚集的影响及其可能机制.方法:建立大鼠的高脂血症模型,同时连续i.g.给予白藜芦醇(50mg· kg-1·d-1)或空白溶媒30 d,测定大鼠血浆TC、TG、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、丙二醛(MDA)、超氧化物歧化酶(SOD)、NO、内皮一氧化氮合酶(eNOS)、p-选择蛋白、血栓烷B2 (TXB2)和6-酮-前列腺素F1α(6-Keto-PGF1α),ADP诱导的血小板5 min最大聚集率.结果:与高脂模型组比较,高脂饲料白藜芦醇组大鼠在连续i.g.给予白藜芦醇(50 mg·kg-1·d-1)30 d后,大鼠血浆TG、TC、LDL-C含量均下降,分别下降19％、31％、51％,HDL-C含量增加1.33倍;SOD和eNOS活力升高,NO和6-Keto-PGF1α含量增加,MDA、p-选择蛋白、TXB2含量降低,ADP诱导的血小板5 min最大聚集率降低.结论:白藜芦醇能有效降低血小板聚集,可能是通过降低血脂水平,防止脂质过氧化和保护内皮细胞完整,影响NO合成,维持血浆或组织中的TXA2和PGI2平衡及细胞内外的钙离子平衡等多环节来发挥作用.     

Asymmetric dimethyl-L-arginine (ADMA): a possible link between homocyst(e)ine and endothelial dysfunction

Hyperhomocyst(e)inemia is associated with an increased risk for atherosclerotic disease and venous thromboembolism. The impact of elevated plasma homocysteine levels seems to be clinically relevant, since the total cardiovascular risk of hyperhomocyst(e)inemia is comparable to the risk associated with hyperlipidemia or smoking. There is substantial evidence for impairment of endothelial function in human and animal models of atherosclerosis, occurring even before development of overt plaques. Interestingly endothelial dysfunction appears to be a sensitive indicator of the process of atherosclerotic lesion development and predicts future vascular events. NO is the most potent endogenous vasodilator known. It is released by the endothelium, and reduced NO bioavailability is responsible for impaired endothelium-dependent vasorelaxation in hyperhomocyst(e)inemia and other metabolic disorders associated with vascular disease. Substances leading to impaired endothelial function as a consequence of reduced NO generation are endogenous NO synthase inhibitors such as ADMA. Indeed there is accumulating evidence from animal and human studies that ADMA, endothelial function and homocyst(e)ine might be closely interrelated. Specifically elevations of ADMA associated with impaired endothelium-dependent relaxation were found in chronic hyperhomocyst(e)inemia, as well as after acute elevation of plasma homocyst(e)ine following oral methionine intake. The postulated mechanisms for ADMA accumulation are increased methylation of arginine residues within proteins, as well as reduced metabolism of ADMA by the enzyme DDAH, but they still need to be confirmed to be operative in vivo. Hyperhomocyst(e)inemia, as well as subsequent endothelial dysfunction can be successfully treated by application of folate and B vitamins. Since ADMA seems to play a central role in homocyst(e)ine-induced endothelial dysfunction, another way of preventing vascular disease in patients with elevated homocyst(e)ine concentrations could be supplementation with L-arginine to reverse the detrimental effects of ADMA.     

Effect of simvastatin on endothelium-dependent vaso-relaxation and endogenous nitric oxide synthase inhibitor

AIM: To investigate the effect of simvastatin on endothelium-dependent vasorelaxation and endogenous nitric oxide synthesis inhibitor asymmetric dimethylarginine (ADMA) in rats and cultured ECV304 cells. METHODS: Endothe-lial injury was induced by a single injection of low density lipoprotein (LDL) (4 mg/kg, 48 h) in rats or incubation with LDL (300 mg/L) or oxidative-modified LDL (100 mg/L) in cultured ECV304 cells, and vasodilator responses to acetylcholine (ACh) in the aortic rings and the level of ADMA, nitrite/nitrate (NO) and tumor necrosis factor-alpha (TNF-α) in the serum or cultured medium were determined. And the adhesion of the monocytes to endothe-lial cells and the activity of dimethylarginine dimethylaminohydrolase (DDAH) in the cultured ECV304 cells were measured. RESULTS: A single injection of LDL decreased endothelium-dependent relaxation to ACh, markedly increased the serum level of endogenous ADMA and TNF-α, and reduced serum level of NO. Pretreatment with simvastatin (30 or 60 mg/kg) markedly attenuated inhibition of vasodilator responses to ACh, the increased level of TNF-α and the decreased level of NO by LDL, but no effect on serum concentration of endogenous ADMA. In cultured ECV304 cells, LDL or ox-LDL markedly increased the level of ADMA and TNF-α and potentiated the adhesion of monocytes to endothelial cells, concomitantly with a significantly decrease in the activity of DDAH and serum level of NO. Pretreatment with simvastatin (0.1, 0.5, or 2.5 μmol/L) markedly decreased the level of TNF-α and the adhesion of monocytes to endothelial cells, but did not affect the concentration of endogenous ADMA and the activity of DDAH. CONCLUSION: Simvastatin protect the vascular endothelium against the damages induced by LDL or ox-LDL in rats or cultured ECV304 cells, and the beneficial effects of simvastatin may be related to the reduction of inflammatory cytokine TNF-α level.     

松针原花青素对高脂大鼠血清中SOD活性、MDA含量的影响

目的探讨松针原花青素对Wistar高脂大鼠血清中超氧化物歧化酶（SOD）、丙二醛（MDA）的影响。方法将40只约40天龄雄性Wistar大鼠随机分为普通饮食组（A）、高脂对照组（B）、高脂＋松针原花青素低（C）、高剂量组（D）,低剂量组100mg／（kg·d）,高剂量组300rag／（kg·d）,每组10只。分别于0、4、8周眦静脉取血测定血清中SOD、MDA的含量。结果8周末时,D组大鼠血清中sOD含量较B组明显升高（P〈0．05）,MDA水平较B组明显降低（P％0．05）;而C组大鼠血清中SOD含量较B组有所升高,差异无统计学意义（P〉0．05）,MDA含量较B组有所降低,差异无统计学意义（P〉0．05）。结论松针提取物具有减缓Wistar大鼠动脉粥样硬化形成的作用,这可能与其提高大鼠血清sOD活性、阻抑MDA升高、减低对血管内皮细胞损伤及保护血管内皮功能等作用有关。较高剂量的松针原花青素能有效改善大鼠的抗氧化能力,原花青素提取物具有降低血液MDA含量、提高血清SOD活力的作用,对其作用机制的进一步研究,可为动脉粥样硬化的治疗提供新的思路和依据。