绞股蓝总皂甙对氧自由基所致脑血管痉挛的保护作用

研究绞股蓝总皂甙（GPS）对外源性氧自由基所致家兔脑基底动脑损伤的保护作用，外源性氧自由基由电解克氏液产生，电解后，脑基底动脉灌注压及血管壁丙二醛（MDA）含量明显升高，脑基底动脉内皮舒张作用，亚硝酸盐及超氧化物歧化酶（SOD）活性明显降低，GPS25、50、100μg／mL可浓度依赖性地抑制氧自由基诱发脑血管收缩作用，此外GPS100μg／mL还具有明显抑制血管壁MDA生成，保护SOD活性的作用。     

蜂胶总黄酮对全脑缺血再灌注大鼠脑血管舒张功能的影响

目的探讨蜂胶总黄酮(Tota1 flavonoids of propoli,TFP)对全脑缺血再灌注大鼠离体脑基底动脉舒张功能的影响及机制。方法采用四血管阻断法制备大鼠全脑缺血再灌注模型;断头取脑后取基底动脉,采用微血管离体灌流实验,以1μmol·L-1 PE预收缩血管后,观察累积浓度的TFP(0.011~2.7 g·L-1)对大鼠离体脑基底动脉的舒张作用。结果在全脑缺血再灌注大鼠,TFP(0.011~2.7 g·L-1)对内皮完整的离体脑基底动脉具有浓度依赖性舒张作用,其最大舒张率为(89.4±3.1)%,与灯盏花素组比较无显著差异(P0.05);去除血管环内皮后,TFP的最大舒张率降至(33.5±4.5)%,与内皮完整组比较明显降低(P0.01);在内皮完整的基底动脉环,用L-NAME+Indo预孵育后,TFP的最大舒张率降为(48.4±3.9)%,与未孵育内皮完整组比较明显降低(P0.01),但仍显著高于去内皮组(P0.01)。结论 TFP对全脑缺血再灌注大鼠离体脑基底动脉具有部分内皮依赖性舒张作用,并且其内皮依赖性舒张作用有EDHF的参与。     

五种中药提取物的血管活性作用实验研究

目的:观察川芎、大蓟、元参、红花和绞股蓝抽提物的血管活性作用。同时研究了绞股蓝的正丁醇、氯仿及水提取物对离体血管的影响。方法:实验是在有内皮和无内皮的离体大鼠主动脉上完成的。离体大鼠主动脉置于浴槽内,各种中药提取物所引起的血管张力改变被测定。结果:除红花外,其他4种中药引起剂量依赖性舒张作用,内皮存在时舒张反应更明显。绞股蓝的正丁醇提取物引起内皮依赖性扩张反应。而氯仿及水提取物无血管活性作用。结论:川芎、大蓟、元参、绞股蓝可引起内皮源舒张因子增加。红花无此作用。     

白藜芦醇对大鼠腹主动脉的舒张作用及其机制探讨

目的:研究白藜芦醇(RVT)对大鼠腹主动脉离体血管的舒张作用特点并探讨其机制。方法:用常规离体血管灌流法灌流大鼠腹主动脉环,测定血管环张力的变化。结果:①白藜芦醇以浓度依赖性舒张NE引起的内皮完整与去内皮血管环收缩,最大舒张幅度分别为(89.5±6.6)%,(60.6±6.3)%,两组各浓度下对应舒张百分比比较,均有显著性差异(n=6,P<0.05)。②在高钾所致的主动脉环收缩反应中,RVT呈浓度依赖性舒张KCl引起的内皮完整的血管环收缩,最大舒张幅度为(80.1±8.3)%;RVT在浓度低于10-5mol/L时对去内皮血管环无明显舒张作用,10-4mol/L RVT可使去内皮血管环达到最大舒张,舒张幅度为(54.2±7.7)%(n=6,P<0.05),RVT在累积浓度大于7×10-5mol/L时,可使去内皮血管环最大舒张(n=6,P<0.05)。③RVT能够拮抗NE诱发的依赖于内钙的收缩反应,而对外钙所致收缩无抑制。结论:白藜芦醇对NE和高钾所致的大鼠离体腹主动脉环的收缩具有舒张作用,既有内皮依赖性又有非内皮依赖性的舒血管效应,其机制可能与内皮依赖性舒血管物质和直接抑制PLC/IP3传导途径,促进内钙释放有关。     

喀什小檗果实水提物对大鼠离体胸主动脉环的舒张作用

目的研究喀什小檗果实水提物对SD大鼠离体胸主动脉环的舒张作用。方法采用离体血管灌流实验方法,观察喀什小檗果实水提物(10～5 000 mg/L)对SD大鼠离体胸主动脉环张力的影响。结果喀什小檗果实水提物对内皮完整和去内皮的离体血管环均有浓度依赖性的舒张作用,当质量浓度在1000～5 000 mg/L时差异有统计学意义(P0. 01)。结论喀什小檗果实水提物具有非内皮依赖性的舒张血管作用。     

杜仲叶醇提取物血管舒张作用的机制研究

目的:研究杜仲叶醇提取物(alcoholextractiveofFoliumEucommiae,AEFE)对家兔离体主动脉血管的舒张作用及其机制。方法:采用家兔离体主动脉血管条固定于灌流肌槽中记录其张力变化。结果:AEFE对血管条静息张力无影响,对高钾预收缩的动脉条无明显舒张作用,但可使Phe预收缩的动脉条明显舒张,且具剂量依赖关系(r=0.997,P<0.001),AEFE的半抑制浓度(IC50)为16.26mg/ml。去内皮和10-3mol/L左旋硝基精氨酸可减弱AEFE的血管舒张作用,而10-4mol/L吲哚美辛则无明显影响。10-4mol/L普奈洛尔使小剂量的AEFE呈现收缩作用(此收缩作用可被哌唑嗪阻断),大剂量才表现舒张效应。结论:AEFE通过促进内皮细胞释放一氧化氮(NO)和直接激活β受体产生舒张血管效应。     

刺五加注射液对氧自由基损伤猪离体冠状血管舒张功能的保护作用

目的研究刺五加注射液对外源性氧自由基(OFR)所致猪冠状动脉内皮损伤的保护作用.方法以内皮依赖性舒血管物质--P物质(SP)为诱导剂,观察猪冠状动脉环暴露于OFR发生系统(H2O2/FeSO4和Xan/XO)后动脉环对SP诱导的舒张反应,以及刺五加注射液对上述舒张反应的影响,并以OFR清除剂过氧化氢酶(CAT)作对照.结果冠状动脉环暴露于H2O2(0.8mmol/L)/FeSO4(0.2mmol/L)系统30min后,SP诱导的内皮依赖性舒张反应显著减弱,刺五加能浓度依赖性地改善冠状血管舒张功能;刺五加10mg/ml时与CAT组比较差异无显著性;刺五加(10mg/ml)和CAT(25mg/L)均能对抗Xan(4.2×10-4mmol/L)/XO(0.025u/ml)系统对冠状血管的损伤.结论刺五加注射液能使冠状血管内皮免受氧自由基损伤,保护冠状血管的舒张功能.     

枸杞多糖对有机磷所致大鼠血管内皮功能损伤的保护作用

目的:探讨枸杞多糖(LBP)对有机磷(PO)所致大鼠血管内皮功能损伤的保护作用。方法:以大鼠离体胸主动脉血管环(EVAPVR)为实验对象,以PO为损伤药物,以LBP为保护药,检测血管内皮依赖性舒张反应(EDRR)。结果:LBP明显减轻了PO对血管EDRR的抑制作用(均P<0.05)。结论:LBP对PO所致的大鼠血管内皮功能损伤有明显的保护作用。     

苦碟子注射液对大鼠离体胸主动脉环的作用

目的：探讨苦碟子注射液对离体大鼠胸主动脉血管环的作用,初步建立苦碟子注射液活性检测方法。方法：采用离体血管灌流方法,观察苦碟子注射液对血管环的直接作用、对肾上腺素和氯化钾所引发收缩作用的影响。结果：各浓度苦碟子注射液对基础状态的完整内皮和无内皮血管环均无舒张作用,对氯化钾引发的血管环收缩无明显的舒张作用,对去氧肾上腺素引发的血管环收缩有舒张作用。结论：苦碟子注射液对去氧肾上腺素预收缩的内皮完整血管环有舒张作用。离体主动脉环灌流实验简单、直观、可量化,可以作为检测苦碟子注射液活性的方法。     

绞股蓝丹对小鼠脑缺血再灌注损伤的脑保护作用

目的 :探讨绞股蓝丹对脑缺血再灌注损伤脑保护的作用机制。方法 :采用小鼠颈总动脉结扎再灌注模型 ,测定脑匀浆中丙二醛 (MDA)、一氧化氮 (NO)含量、总抗氧化能力 (T_AOC)及过氧化氢酶 (CAT)活性 ,探讨预防性给予绞股蓝丹对脑组织的保护作用机理。结果 :绞股蓝丹能明显提高小鼠脑缺血再灌注损伤脑组织的T_AOC和CAT活性 ,明显抑制损伤脑组织中的MDA升高。结论 :绞股蓝丹可通过抗氧化机制达到脑保护功能。     

补肾中药对关节软骨的保护作用机制研究进展

补肾中药治疗骨关节炎主要通过减轻损伤、延缓退变及促进软骨分化和修复两方面起作用,其机制包括（1）抑制促分解细胞因子的表达;（2）阻止自由基的生成,抑制NOS的活性,减少NO的生成;（3）对关节软骨细胞凋亡的调控;（4）对关节软骨细胞增殖的作用;（5）对关节软骨基质的作用;（6）提高促合成性细胞因子的表达等方面。     

红花提取物预处理对缺血再灌注心肌的影响

目的；观察红花提取物预处理对心肌缺血再灌注损伤的影响。方法：采用离体心脏Langendorff装置，观测经红花提取物预处理后心功能指标和冠脉流量的改变；同时采用在体心脏结扎左冠状动脉前降支制备心肌缺血再灌注模型，在心肌缺血前各组心脏分别用红花提取物或维拉帕米治疗，并贯穿于实验全过程中。缺血再灌注组实施20分钟缺血和40分钟再灌注。分别检测心肌组织中的丙二醛（MDA）含量、超氧化物歧化酶（SOD）和心肌激酶（CK）活性、心率等变化。结果：红花提取物能减少缺血再灌注心肌中的MDA含量，降低SOD和CK活性．减慢心率，改善心功能指标。结论：红花提取物能改善心功能，保护缺血心肌，其机制可能与其清除自由基，抑制自由基的释放有关。     

Evaluation of antioxidant activity of Cassia siamea flowers

The study was aimed at evaluating the antioxidant activity of alcoholic extract of Cassia siamea Lam. (Fabaceae) flowers. The extract was found to contain a large amount of polyphenols and also exhibited an immense reducing ability. At a concentration of 250 microg/ml, 96% of DPPH radicals and at 500 microg/ml, 42.7, 32.7 and 64.5% of O2-, H2O2 and NO respectively could be scavenged by C. siamea flower extract. The extract also inhibited OH radical induced oxidation of protein (BSA) and LPO in murine hepatic microsomes. The determination of metal chelating capacity of the extract indicated chelating of metal ions (Fe2+) to be a putative mechanism implicated in the inhibition of OH radical-induced BSA oxidation and LPO. C. siamea flower extract also exhibited a significant antioxidant activity in acute oxidative tissue injury animal model constituted by CCl4 induced hepatotoxicity. Oral administration of the extract at a dose of 50-150 mg/kg of body weight significantly protected from CCl4 induced elevation in AST and ALT in the serum, elevation in hepatic LPO, depletion of hepatic GSH and decrease in the activities of hepatic antioxidant enzymes: SOD, CAT and GPX. The extract also protected against histopathological changes produced by CCl4 such as necrosis, fatty changes, ballooning degeneration, etc. The data obtained in the present study suggests that the alcoholic extract of C. siamea flowers have potent antioxidant activity against free radicals, prevent oxidative damage to major biomolecules and afford significant protection against oxidative damage in the liver.     

红花水提物对ox-LDL损伤心肌微血管内皮细胞的 保护作用及ESR谱研究

目的：观察红花水提物对氧化低密度脂蛋白(ox-LDL)致体外培养大鼠乳鼠心肌微血管内皮细胞损伤的保护作用，并初步探讨其抗氧化作用机制。方法：采用第3代大鼠乳鼠心肌微血管内皮细胞，用红花水提物预处理(500，100，20 mg·L-1)24 h后，ox-LDL(100 mg·L-1)孵育24 h进行损伤，实验结束后取上清液，测定细胞上清液中乳酸脱氢酶(LDH)、丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、一氧化氮(NO)、一氧化氮合酶(NOS)和黄嘌呤氧化酶(XOD)活性，用自旋捕集技术结合电子自旋共振波谱技术(electron spin resonance，ESR)检测各组细胞悬液中氧自由基信号的强弱。结果：红花水提物各剂量组能够明显减少内皮细胞LDH的释放，降低培养液中MDA含量和XOD的活性，同时提高SOD，NO，NOS和GSH-Px的活性，使细胞悬液中的ESR自由基信号明显减弱。结论：红花水提物具有抗ox-LDL致体外培养大鼠乳鼠心肌微血管内皮细胞损伤的作用，其机制与其减少氧自由基产生、增强自由基的清除、增强内源性抗氧化剂的活性，使高毒性的自由基转化成无害物质等有关。     

Effects of phenylpropanoid and iridoid glycosides on free radical-induced impairment of endothelium-dependent relaxation in rat aortic rings.

The protective effect of phenylpropanoid glycosides, forsythoside B and alyssonoside, and the iridoid glycoside lamiide, isolated from the aerial parts of Phlomis pungens var. pungens, against free radical-induced impairment of endothelium-dependent relaxation in isolated rat aorta was investigated. Aortic rings were exposed to free radicals by the electrolysis of the physiological bathing solution. Free radical-induced inhibition of the endothelium-dependent relaxation in response to acetylcholine was countered by incubation of the aortic rings before electrolysis with the aqueous extract (200 microg/ml), phenylpropanoid fraction (100 microg/ml) and iridoid fraction (150 microg/ml) of P. pungens var. pungens. Major components of the phenylpropanoid fraction forsythoside B and alyssonoside also prevented the inhibition of the acetylcholine response, at 10(-4) M concentration. However, the major component of iridoid fraction lamiide was found ineffective at the same concentration. The protective activity of phenylpropanoid glycosides against the free radical-induced impairment of endothelium-dependent relaxation may be related to their free radical scavenging property.     

The effect of Ginkgo biloba extract on mitochondrial oxidative phosphorylation in the normal and ischemic rat heart

Free radical‐induced myocardial damage and impairment of vascular endothelium‐dependent relaxation are amongst the most important mechanisms responsible for ischemic heart injury. Ginkgo biloba leaf extract (GE) has been reported to improve blood circulation in the brain and have a beneficial impact on the cardiovascular system but its cardioprotective effects have not been elucidated yet. Therefore, this study investigated the influence of GE in 70% ethanol (1:5) administered orally to rats on the functions of isolated heart mitochondria under normal and ischemic conditions. Wistar rats were given GE or ethanol (solvent control) at a dosage of 0.32 mL/kg in drinking water for 10 and 18 days, while the control animals received untreated drinking water. Mitochondrial respiration rates were determined oxygraphically. Pyruvate and malate, succinate or palmitoyl‐l ‐carnitine and malate were used as substrates. The GE treatment partially uncoupled mitochondrial oxidation from phosphorylation, reduced the generation of free radicals in the mitochondria, diminished the ischemia‐induced V₃ decrease and the degree of respiration stimulation by exogenous cytochrome c. Thus, these results indicate that GE exerts cardioprotective effects reducing ischemia‐caused impairment of the functions of heart mitochondria. Copyright © 2011 John Wiley & Sons, Ltd.     

Pharmacological mechanisms involved in the vasodilator effects of extracts from Echinodorus grandiflorus

We investigated the vascular effects of a crude aqueous extract (AEEG) of Echinodorus grandiflorus (Alismataceae) using the in vitro experimental models of the rabbit isolated aorta and perfused kidney. Echinodorus grandiflorus, a native semi-aquatic plant widely distributed in Brazil, has been extensively used in Brazilian folk medicine for the treatment of high blood pressure and inflammatory diseases. The bolus injection of AEEG (0.1-10 mg) into the rabbit renal circulation pre-contracted with norepinephrine induced marked and dose-dependent vasodilator responses (maximum of 37+/-4%; n=6; P<0.001), which was similar to that induced by injection of 10 mmol acetylcholine (41+/-3%). Moreover, AEEG elicited a significant and concentration-dependent relaxation in the endothelium-intact, but not endothelium-denuded aortic rings, reaching the maximum of 81+/-5% (n=7, P<0.001). Inhibition of the nitric oxide-cGMP pathway with L-NAME (100 microM) or Methylene Blue (20 microM) reduced maximum relaxation induced by AEEG from 81+/-5% to 46+/-3 and 45+/-3%, respectively (n=7, P<0.001). A similar reduction was obtained with the incubation of the aortic rings with the selective PAF receptor antagonist WEB 2086 (10 microM) (from 81+/-5% to 55+/-3%; n=7; P<0.01). Conversely, blockade of muscarinic receptors with atropine (10 microM) did not affect the vasodilator effects of AEEG, while inhibition of the enzyme cyclooxigenase not only did not block, but rather potentiated vasodilation induced by AEEG (n=7, P<0.001). Finally, blockade of Ca(2+)- and ATP-activated K(+) channels using the specific blockers charydbotoxin (100 nM) and glibenclamide (3 microM), respectively, did not modify aortic relaxation induced by AEEG. We conclude that water-soluble extracts from leaves of Echinodorus grandiflorus elicit an endothelium-dependent, nitric oxide and PAF receptor-mediated vasodilation in rabbit aortic rings, which does not appear to involve the generation of vasodilating prostaglandins or the activation of K(+) channels. This potent vasodilator effect of the extracts was confirmed in the isolated rabbit renal circulation.     

银杏叶提取物对谷氨酸诱导的兔视网膜NO水平及细胞凋亡的影响

目的 :探讨银杏叶提取物 (extract of ginkgo biloba ,EGB)对谷氨酸诱导的兔视网膜NO水平及细胞凋亡的影响作用。方法 :利用谷氨酸兔玻璃体内注射 ,诱导视网膜细胞凋亡的模型 ,眼球后注射不同剂量的EGB ,采用分光光度法测定兔视网膜NO水平 ,琼脂糖凝胶电泳分析视网膜细胞DNA断裂。结果 :实验对照组视网膜的NO的水平与空白对照组相比显著增加 (P<0.001) ,EGB大剂量治疗组视网膜NO水平比实验对照组显著降低 (P<0.001) ,EGB小剂量治疗组视网膜的NO水平与实验组相比轻度降低 ,但无统计学差别。EGB大剂量治疗组和空白对照组视网膜细胞无DNA凋亡样断裂 ,而实验组和EGB小剂量治疗组视网膜细胞DNA凋亡样断裂。结论 :银杏叶提取物可能通过抑制谷氨酸诱导的兔视网膜NO自由基的产生而抑制细胞凋亡 ,对谷氨酸诱导的兔视网膜损伤具有重要保护作用。     

北虫草对正己烷所致大鼠损伤的保护作用

采用正己烷急性吸入模型研究北虫草的药效和正己烷的损伤作用。结果表明：北虫草具有抗脂质过氧化作用;正己烷的急性吸入可引起或增强机体活性氧自由基的损伤反应,导致脂质过氧化损伤,这可能是正己烷对机体毒性作用的机制之一。     

橙皮苷对羟自由基引发红细胞膜损伤的影响

 目的：建立羟自由基(·OH)引发的人红细胞膜氧化损伤实验模型，研究橙皮苷对红细胞膜氧化损伤的保护作用。方法：以Fenton反应产生的羟自由基引发人红细胞膜氧化损伤，并以此为实验模型研究橙皮苷对红细胞膜氧化损伤的影响。结果：·OH能引起红细胞膜脂质过氧化，丙二醛(MDA)含量显著升高；膜脂流动性下降以及膜重封闭能力减小。而红细胞膜经一定量橙皮苷预先处理后，膜MDA含量明显减少；膜脂流动性和膜重封闭能力可显著提高。结论：橙皮苷对·OH引起的红细胞膜氧化损伤有一定的保护作用。