花卷茶提取物对高胆固醇血症大鼠血脂和内皮功能的影响

目的研究花卷茶提取物对高胆固醇血症大鼠血脂和内皮功能的影响及机制。方法雄性SD大鼠高脂饲养4周诱发高胆固醇血症,其中实验组在高脂饲料饲养2周后开始每日灌胃给予不同剂量的花卷茶系列之十两茶水提物（50、100和200mg.kg-1）,持续2周。实验结束后,颈动脉取血测定血脂、一氧化氮（NO）、非对称二甲基精氨酸（ADMA）和丙二醛（MDA）含量;分离胸主动脉检测血管内皮依赖性舒张功能。结果十两茶提取物能呈剂量依赖性降低高脂血症大鼠血清总胆固醇和低密度脂蛋白及甘油三酯水平。十两茶提取物能显著改善高脂所诱导的血管内皮舒张功能障碍,降低血浆ADMA和MDA含量以及增加NO水平,且呈剂量依赖性。结论花卷茶系列之十两茶提取物具有降低血脂和保护血管内皮功能作用,其作用与抑制脂质过氧化、调节ADMA/NO系统有关。     

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。     

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。     

小剂量阿司匹林对LDL所致内皮损伤的保护作用与内源性一氧化氮合酶抑制物的关系

目的研究阿司匹林对低密度脂蛋白(LDL)诱导的血管内皮损伤的保护作用与内源性一氧化氮合酶抑制物的关系.方法 SD大鼠在乙醚麻醉下,舌下静脉注射人血清LDL(4 mg·kg-1)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)和肿瘤坏死因子α(TNF-α)的含量,以及二甲精氨酸二甲胺水解酶(DDAH)活性,并观察离体胸主动脉环的内皮依赖性舒张反应.结果单次静脉注射LDL(4 mg·kg-1)显著抑制乙酰胆碱(ACh)诱导的内皮依赖性舒张,增加血液中ADMA、MDA和TNF-α水平,降低DDAH活性.两个剂量阿司匹林(30或100 mg·kg-1)均能显著减轻LDL所致ACh诱导内皮依赖性舒张的损伤,但较大剂量阿司匹林作用较小剂量阿司匹林组作用为弱;两个剂量阿司匹林也能抑制LDL所致MDA和TNF-a浓度升高;小剂量阿司匹林能显著抑制ADMA浓度升高和增加DDAH活性,但较高剂量的阿司匹林对ADMA浓度和DDAH活性无影响.结论小剂量阿司匹林对LDL诱导的血管内皮细胞损伤有保护作用,其保护作用与增加DDAH活性和降低ADMA浓度有关.     

不对称性二甲基精氨酸与脑梗死的相关性研究

内皮依赖性血管舒张反应功能障碍是动脉粥样硬化的特征性表现.一氧化氮(nitric oxide,NO)对维持内皮正常功能有重要作用.不对称性二甲基精氨酸(asymmetric dimethylarginine,ADMA)为一氧化氮合酶(nictric oxide synthase,NOS)抑制剂,它能竞争性抑制NOS活性,减少NO生成.在多种病理生理状况下ADMA水平显著升高,内皮细胞NOS活性降低,NO合成减少,导致血管内皮功能不全~([1]).本研究旨在通过检测脑梗死患者ADMA水平,探讨ADMA与脑梗死的相关性.     

二苯乙烯苷对动脉硬化大鼠主动脉一氧化氮合酶表达及舒张作用的影响

目的探讨二苯乙烯苷(TSG)对动脉粥样硬化大鼠主动脉一氧化氮合酶(NOS)表达的影响及对主动脉的舒张作用。方法SD大鼠65只,(?),随机分为6组:正常对照组、模型组、辛伐他汀组、TSG 120 mg·kg~(-1)·d~(-1)组、TSG 60 mg·kg~(-1)·d~(-1)组及TSG 30 mg·kg~(-1)·d~(-1)组。采用高脂饲料喂饲+VitD_3复制大鼠动脉粥样硬化模型,造模12 wk后抽样检测大鼠主动脉,以大鼠动脉粥样硬化斑块形成为造模指标。经治疗6 wk后,分离主动脉,-70℃保存,Western blot检测主动脉组织中NOS含量,RT-PCR检测大鼠主动脉内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)mRNA表达,同时观察TSG对大鼠离体主动脉血管环内皮依赖性血管舒张作用的影响。结果与模型组相比,辛伐他汀组和TSG各剂量组均能显著增加主动脉组织eNOS表达及降低主动脉组织iNOS表达,并呈剂量依赖性。TSG抑制去甲肾上腺素(NA)诱发的内皮依赖性血管收缩、增强乙酰胆碱(Ach)内皮依赖性血管舒张;TSG的血管舒张作用可被NO前体物L-精氨酸增强,而NOS抑制药L-硝基精氨酸甲酯可部分削弱之。结论TSG能上调其主动脉eNOS和下调iNOS表达,并能使内皮依赖性血管舒张,这可能与TSG抗AS作用的机制有关。     

依达拉奉对LPC所致兔胸主动脉内皮功能的影响及机制

目的探讨依达拉奉(edaravone,Eda)对溶血磷脂酰胆碱(lysophosphatidylcholine,LPC)所致家兔血管内皮损伤的影响及机制。方法家兔胸主动脉环分别与LPC(5 mg.L-1)和Eda(25～100μmol.L-1)单独孵育或共孵育,分别检测乙酰胆碱诱导的内皮依赖性舒张反应和硝普钠诱导的非内皮依赖性舒张反应,血管组织中一氧化氮(nitric oxide,NO)和丙二醛(malonaldehyde,MDA)含量以及超氧化物歧化酶(superoxide dismutase,SOD)的活性。结果 5 mg.L-1LPC孵育血管环30 min,明显抑制了乙酰胆碱诱导的内皮依赖性舒张反应,但没有影响硝普钠诱导的非内皮依赖性舒张反应,降低了血管组织中NO含量和SOD活性而增加了MDA含量。25～100μmol.L-1Eda分别孵育血管环15min,再与5 mg.L-1LPC共同孵育30 min,明显改善LPC所致的血管舒张功能的损害,升高了血管组织中NO含量和SOD活性而降低了MDA含量。结论 Eda对LPC所致的血管内皮依赖性舒张功能的损伤具有明显的保护作用,该效应可能与其抗氧化作用有关。     

洛伐他汀对溶血性磷脂酰胆碱引起的离体血管内皮损伤的保护作用

目的探讨洛伐他汀（Lov）对溶血性磷脂酰胆碱（LPC）所致血管内皮损伤的保护作用及机制。方法利用家兔离体胸主动脉环和培养的人内皮细胞模型,分别观察洛伐他汀对LPC致离体血管环内皮依赖性舒张反应的损伤及对内皮细胞合成NO的损伤的保护作用。血管环分别与LPC（4 mg.L-1）和洛伐他汀（0.025、0.05、0.1μmol.L-1）单独孵育和共孵各15 min,分别检测乙酰胆碱（ACh）诱导的内皮依赖性舒张（EDR）反应及硝普钠诱导的非内皮依赖性舒张（EDR）反应及血管组织中的脂质过氧化物产物丙二醛（MDA）的含量。在培养的人内皮细胞和培养基中分别加入LPC和洛伐他汀,分别检测LPC和洛伐他汀对内皮细胞中一氧化氮（NO）含量和一氧化氮合酶（eNOS）的影响。结果LPC（4 mg.L-1）与血管环孵育15 min,引起了血管EDR的显著降低,最大舒张比值较对照组明显减小（P〈0.01）,洛伐他汀剂量依赖性地减轻了LPC对血管EDR的损伤作用,其最大舒张比值较LPC损伤组明显增加,（P〈0.01）。LPC和洛伐他汀对硝普钠诱导的非内皮依赖性舒张反应无明显影响。LPC引起了血管组织中MDA浓度明显升高,与对照组相比有显著性差异（P〈0.01） 不同浓度的洛伐他汀与血管环预孵后再与LPC孵育,剂量依赖性地减少了LPC所增加的MDA浓度,与LPC损伤组比较有显著差异（P〈0.01）。LPC与培养的内皮细胞孵育,导致了内皮细胞NO含量和eNOS活性的降低,不同浓度的洛伐他汀与内皮细胞预孵后再与LPC孵育,剂量依赖性地提高eNOS活性和NO的含量。结论LPC能直接抑制血管的EDR反应,洛伐他汀能剂量依赖性地拮抗LPC对EDR反应的抑制作用。其机制可能与LPC触发脂质过氧化反应,从而抑制血管内皮细胞NO的合成和增加NO的消耗有关,洛伐他汀通过抗氧化而保护血管内皮细胞的功能。     

3,4,5,6-四羟基(口山)酮对高糖所致血管内皮依赖性舒张功能减退的保护作用

目的:观察3,4 ,5 ,6 - 四羟基口山酮对高糖所致血管内皮依赖性舒张功能减退的保护作用。方法:在大鼠离体胸主动脉环,用高浓度葡萄糖(2 5mmol·L-1)孵育2 4h ,检测乙酰胆碱诱导的血管内皮依赖性舒张反应;人脐静脉内皮细胞株(ECV30 4 )用高浓度葡萄糖(30mmol·L-1)培养4 8h ,测定培养液中乳酸脱氢酶(LDH)活性、一氧化氮(NO)及细胞脂质过氧化物丙二醛(MDA)含量。结果:3,4 ,5 ,6 - 四羟基口山酮(1、3和10 μmol·L-1)能显著抑制高糖所致的舒血管效应减退,并且呈剂量依赖性。3,4 ,5 ,6 - 四羟基口山酮(1、3和10 μmol·L-1)能显著抑制高糖所致的内皮细胞LDH泄漏、NO释放和MDA生成的增加。结论:3,4 ,5 ,6 - 四羟基口山酮对高糖所致的血管内皮依赖性舒张功能减退有保护作用,其保护作用与抑制脂质过氧化减少血管内皮细胞损伤有关。     

血府逐瘀汤对动脉粥样硬化大鼠血清非对称性二甲基精氨酸水平的影响

目的观察血府逐瘀汤对动脉粥样硬化大鼠血清非对称性二甲基精氨酸(asymmetric dimethylarginine,ADMA)的影响,并探讨血府逐瘀汤抗动脉粥样硬化的机制。方法24只大鼠随机分为对照组(n=8)、模型组(n=8)、血府逐瘀汤组(n=8)。采用高脂喂养大鼠动脉粥样硬化模型,以血府逐瘀汤对该模型进行干预。观察各组大鼠血清ADMA、NO浓度、主动脉组织形态学的变化。结果模型组大鼠主动脉粥样硬化改变明显;血府逐瘀汤组大鼠主动脉粥样硬化病理改变优于模型组;模型组大鼠血清ADMA水平明显高于血府逐瘀汤组(P=0.00),而NO水平明显低于血府逐瘀汤组(P=0.00)。血府逐瘀汤组大鼠血清ADMA及NO水平与对照组无明显差别(P分别为0.24、0.16)。大鼠血清ADMA与NO水平呈负相关关系(r=-0.73,P=0.00)。结论血府逐瘀汤能降低动脉粥样硬化大鼠血清ADMA浓度,血府逐瘀汤抗大鼠动脉粥样硬化作用与ADMA有关,降低血清ADMA水平可能是其中的一个重要机制。     

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.     

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.     

生姜提取物对大鼠视网膜缺血-再灌注损伤的保护作用研究

目的:研究生姜提取物对大鼠视网膜缺血-再灌注损伤的保护作用。方法:实验分为3组,即正常对照、模型及生姜提取物(400mg·kg-1)组。采用前房灌注生理盐水60min复制视网膜缺血-再灌注模型。复制模型前5天开始,生姜提取物组灌胃生姜提取物,每天分2次给药,模型组大鼠灌胃蒸馏水,复制模型后仍继续原给药方案。于复制模型后12、24、48、72h测定大鼠视网膜中超氧化物歧化酶(SOD)活性和丙二醛(MDA)、一氧化氮(NO)含量的变化;电镜观察视网膜超微结构。结果:与模型组比较,生姜提取物组大鼠视网膜SOD活性显著增强,MDA、NO含量显著减少(P<0.05);视网膜超微结构损伤有所减轻。结论:生姜提取物可调控SOD活性及MDA、NO含量,改善超微结构而保护视网膜。     

RAPID REVERSAL OF ENDOTHELIAL DYSFUNCTION IN HYPERCHOLESTEROLAEMIC RABBITS TREATED WITH SIMVASTATIN AND PRAVASTATIN

1. The main objective of the present study was to verify the speed with which two 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, simvastatin and pravastatin, could revert endothelial cell dysfunction in hypercholesterolaemic rabbits. An attempt was also made to correlate the plasma cholesterol level and the tissue cholesterol and malondialdehyde (MDA) contents of the aortae with the endothelium-dependent relaxation on the assumption that any endothelial dysfunction could be rapidly and partially reversed, even in the presence of relatively high serum cholesterol levels. 2. Ninety-one male New Zealand white rabbits were randomly assigned to hypercholesterolaemic (control), simvastatin or pravastatin groups. All rabbits were fed a diet supplemented with cholesterol (0.5%) and coconut oil (2%) for 8 weeks. Simvastatin (10 and 20 mg/day) and pravastatin (15 and 30 mg/day) were administered 6, 4 and 2 days before the end of the experiment. At the end of the 8th week, animals were killed and the aortae were removed for histological examination as well as for the measurement of cholesterol and MDA contents and for endothelium-dependent relaxation studies. 3. The results showed that significant improvement in endothelium-dependent relaxation was obtained only with pravastatin and only with 4 or 6 days of administration. In these cases, the cholesterol and MDA contents of the vessel wall were reduced, although no significant changes were observed in plasma total cholesterol. Higher doses of the drugs did not alter these results. 4. We conclude that pravastatin enhances endothelium-dependent relaxation when administered to cholesterol-fed rabbits, probably via an anti-oxidant action. This effect, which was observed to start on the 4th day of drug administration, may represent a new therapeutic approach for the treatment of acute coronary syndromes in hypercholesterolaemic patients.     

气滞血瘀模型大鼠红细胞膜生物学研究

目的从血液流变学和红细胞膜生物学变化探讨气滞血瘀证在红细胞膜上的生物学差异。方法20只Wistar大鼠,随机分为空白组及气滞血瘀组,每组10只。采用声光电等复合刺激对气滞血瘀组连续造模15d后,取血测定血液流变学指标以及红细胞膜组分相关指标。结果与空白组比较,气滞血瘀组大鼠体重显著降低;全血黏度、血浆黏度和红细胞变形指数部有降低趋势但无显著性;APTT降低极显著（P〈0．01）;PT、FIB和TT无显著变化;Na^＋-K^＋-ATP酶活力及SOD活力均显著降低（P〈0．01,P〈0．05）;唾液酸含量显著降低（P〈0．05）;MDA含量显著升高（P〈0．05）。结论气滞血瘀模型中红细胞膜上Na^＋-K^＋-ATP酶及SOD酶活力降低,并且唾液酸含量降低,但是全血黏度及红细胞变形性等未发生显著变化。但都有相应的趋势出现．可能是本实验中刺激强度较大但刺激时间略短造成的,也有可能和APTT等凝血机制有关,此模型有待进一步探索。     

乌灵菌粉对实验性动脉粥样硬化兔的抗氧化系统及炎症因子的影响

目的 探讨乌灵菌粉对实验性动脉粥样硬化兔的抗氧化系统及炎症因子的影响。方法 建立兔的动脉粥样硬化模型,同时连续给予乌灵菌粉（100 mg·kg^-1·d^-1）12周,测定兔血浆中总胆固醇、甘油三酯（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）、C反应蛋白（CRP）,白介素6,肿瘤坏死因子含量及超氧化物歧化酶（SOD）,谷胱甘肽过氧化物酶（GSH-Px）活力,并观察主动脉病理学形态改变。结果 给予乌灵菌粉可有效减小高脂饲料引起兔动脉粥样硬化斑块的厚度,同时使动脉粥样硬化兔血浆TG、MDA、CRP含量显著下降（P〈0.01）,HDL-C含量、SOD及GSH-Px活力显著升高（P〈0.01）。结论 乌灵菌粉能降低动脉粥样硬化兔TG水平及增加抗氧化酶活力,抑制部分炎性因子的产生来达到降低或缓解动脉粥样硬化的目的。