丹参酮ⅡA磺酸钠对冠心病患者血小板功能的影响

目的:探讨丹参酮ⅡA磺酸钠对冠心病患者血小板功能的影响。方法:按照随机数字表法将88例冠心病患者均分为实验组和对照组,对照组给予常规综合治疗,实验组在此基础上加用丹参酮ⅡA磺酸钠注射液治疗,比较两组患者治疗效果。结果:实验组患者治疗后黏度水平均明显低于对照组,差异有统计学意义(P<0.05);实验组患者治疗后血小板膜糖蛋白CD62p,CD63,PAC-1水平均明显低于对照组,CD42b水平明显高于对照组,差异有统计学意义(P<0.05)。结论:丹参酮ⅡA磺酸钠能够有效改善冠心病患者血液黏度和血小板功能。     

丹参酮ⅡA与丹参酮ⅡA磺酸钠对HepG2细胞的抑制作用

目的 比较丹参酮ⅡA与丹参酮ⅡA磺酸钠对人肝癌HepG2细胞的体外增殖抑制作用.方法 采用改良MTT法测定丹参酮ⅡA与丹参酮ⅡA磺酸钠对HepG2的增殖抑制作用,倒置显微镜下观察两者对HepG2细胞的形态学影响.结果 3.4～27.2 μmol·L~(-1)丹参酮ⅡA对HepG2细胞有明显的增殖抑制作用,并呈时间和剂量依赖性,而对应各浓度丹参酮ⅡA磺酸钠对HepG2细胞均无增殖抑制作用.结论 丹参酮ⅡA对HepG2细胞具有显著增殖抑制作用,其与丹参酮ⅡA磺酸钠在抗肝癌的药效方面可能存在差异.     

丹参酮ⅡA与丹参酮ⅡA磺酸钠对 K562细胞的增殖抑制与诱导分化作用

目的 比较丹参酮ⅡA与丹参酮ⅡA磺酸钠对人白血病K562细胞的体外增殖抑制与诱导分化作用.方法 采用改良MTT法测定两种药物对K562细胞的增殖抑制作用,倒置显微镜下观察其对K562细胞形态的影响,以硝基四氮唑蓝还原试验法,用流式细胞仪测定细胞膜表面的分化抗原CD33和CD11 b,观察丹参酮ⅡA与丹参酮ⅡA磺酸钠对K...     

丹参酮ⅡA与丹参酮ⅡA磺酸钠在小鼠体内的分布

目的考察静脉注射丹参酮ⅡA与丹参酮ⅡA磺酸钠后,二者在小鼠体内的分布行为,证实两者穿透血脑屏障的差异。方法小鼠分别静脉给予丹参酮ⅡA乳剂与丹参酮ⅡA磺酸钠注射液,以HPLC法测定各主要脏器组织中的药物含量。结果丹参酮ⅡA乳剂与丹参酮ⅡA磺酸钠静脉给药后均快速分布至各主要脏器组织,其中以肝脏的药物分布量最高;前者在脑组织中的分布明显高于后者。结论丹参酮Ⅱ比丹参酮ⅡA磺酸钠更易进入血脑屏障,提示丹参酮ⅡA乳剂有望用于脑血管病的预防和治疗。     

丹参酮ⅡA磺酸钠注射液致过敏性休克

患者男,70岁。因反复右上腹痛20d,加剧3h,于2006年6月20日入院。查体:T36.5℃,P99次/min,R23次/min,BP140/96mmHg(1mmHg=0.133kPa),神清、     

丹参酮ⅡA磺酸钠对造影剂引起肾脏损害的作用

目的 探究丹参酮ⅡA磺酸钠的应用是否可以有效改善造影剂给患者带来的肾损伤情况.方法 选取2014年1月至2015年6月在本院接受冠状动脉造影患者82例,随机均分为丹参酮ⅡA磺酸钠治疗研究组和单纯基础治疗对照组,对比分析两组患者治疗后肾功能变化情况.结果 入选患者术后第1、3d呈现肾小球滤过率较低的情况,研究组患者术后第7、10 d的肾小球滤过率显著高于对照组.研究组患者的尿酸水平从(287.2±23.5)μmol/L降低到(224.7±29.9)μmol/L,对照组的尿酸水平从(272.4±28.9)μmol/L降低到(265.9±21.1) μmol/L,研究组术后尿酸水平较对照组显著降低.结论 在KDIGO指南指导下,适量使用丹参酮ⅡA磺酸钠可有效改善造影剂对患者造成的肾损伤,提高患者的生存质量.     

丹参酮ⅡA磺酸钠注射液治疗心血管疾病的作用研究进展

目的总结丹参酮ⅡA磺酸钠注射液对心血管疾病治疗作用的研究进展。方法参阅最近几年的相关资料并进行归纳总结。结果与讨论对近几年丹参酮ⅡA磺酸钠注射液对治疗心血管疾病的临床作用和实验探索进行分析总结,认为丹参酮ⅡA磺酸钠注射液在心血管疾病的治疗过程发挥了显著的疗效。     

丹参酮ⅡA磺酸钠治疗冠心病的临床观察

目的观察丹参酮ⅡA磺酸钠结合常规疗法治疗冠心病的疗效。方法选择经冠脉造影术确诊为冠心病的患者65例,随机分为治疗组39例,对照组26例。对照组采用常规治疗,治疗组加用丹参酮ⅡA磺酸钠注射液治疗。结果治疗组总有效率为92.3%高于对照组的69.2%,差异有统计学意义（P〈0.05）;治疗组超敏C-反应蛋白（hsCRP）水平降低较对照组显著（P〈0.05）。结论丹参酮Ⅱ磺酸钠结合常规疗法治疗冠心病有良好疗效。     

丹参酮ⅡA磺酸钠对腹膜间皮细胞结缔组织生长因子表达的影响

目的观察丹参酮ⅡA磺酸钠对高浓度葡萄糖（高糖）环境中腹膜间皮细胞（PMCs）结缔组织生长因子（CTGF）表达的影响。方法原代培养大鼠PMCs,使用不同浓度葡萄糖作用于PMCs,然后给予丹参酮ⅡA磺酸钠进行干预,采用ELISA方法检测培养液中CTGF蛋白的含量,逆转录聚合酶链反应（RT PCR）检测CTGF mRNA的表达。 结果与对照组比较,高糖作用下PMCs的CTGF表达明显增强（P＜0.01）,丹参酮ⅡA磺酸钠以剂量依赖方式抑制高糖作用下PMCs CTGF表达（P＜0.01）。结论丹参酮ⅡA磺酸钠能抑制高糖对PMCs CTGF的诱导,使PMCs CTGF的表达下调,因而具有抑制细胞外基质聚积、防治腹膜纤维化发生的作用。     

丹参酮Ⅱ-A磺酸钠的药理研究

丹参酮Ⅱ-A磺酸钠(丹参201)是丹参酮Ⅱ-A的新水溶性衍生物。临床试用中对冠心病心绞痛和胸闷的症状有一定疗效,并能改善缺血性心电图。本文进行了丹参201对小鼠缺氧、狗心脏血流动力作用和小鼠体内代谢的研究。腹腔注射200 mg/kg,可显著的延长小鼠在缺氧情况下的存活时间;氧耗速度较对照组稍减慢;其死亡时余存氧含量亦较对照组为低(P<0.05)。小鼠缺氧达到氧含量为6%时,心脏和脑组织中乳酸含量较正常组显著增加,而给丹参201后半小时再进行缺氧实验,组织中乳酸含量不增加,与正常组差异不显著。麻醉狗,一次静脉推注20 mg/kg,出现轻度血压升高,心输出量和左心室作功量稍有增加,心率和外周血管阻力的变化不显著。小鼠静注³⁵S-丹参201后2分钟血中放射活性为75843 cpm/0.1 ml,90分钟已降至3785 cpm/0.1 ml。注后1小时,以肝、肺和肠中放射活性为高;肾、脾、心和胃次之。6和24小时均趋减少。肠内容物中的放射活性在不同时间内均占首位。胆囊中亦较多。24小时内尿和粪中排泄率分别为10.2%和32.0%;24～48小时内分别为4.5%和24.1%;48～72小时内分别为1.8%和19.6%。经非放射性和放射性薄层层析及放射自显影证明,由尿中排出的代谢物,一个为丹参201的原型,另一个为代谢产物,其基本骨架与原型相似,看来是增加了某些极性基团。     

槲皮素对体外血小板与微血管内皮细胞粘附的影响

目的：研究槲皮素（Que)对血小板与人皮肤分离的微血管内皮细胞（MVEC）粘附的影响。方法：用[^3H]-腺嘌呤标记的血小板与MVEC共同孵育,研究Que对血小板对MVEC粘附所起的作用。Que对MVEC上血小板内皮细胞粘附分子（PECAM）表达的影响用酶联免疫法评价。结果：血小板加入MVEC中后立即发生粘附并于30min达到最大值。Que能浓度依赖地抑制血小板粘附,Que 5μmol/L无显著的抑制作用,但Que浓度为10、20和40μmol/L时,抑制率分别为10．5％、20．0％和42．2％。Que与标记的血小板预先孵育30min,也能浓度依赖地抑制其粘附,Que10、20和40μmol/L的抑制率分别为18．2％、29．8％和65．3％,而Que 5μmol/L在两种处理中均无效。当用Que 10-40μmol/L处理MVEC时,Que能浓度依赖地减少MVEC上PECAM的表达,但Que 5μmol/L无显著效果。结论：Que能抑制血小板与MVEC的粘附,此作用可能与减少MVEC上PECAM的表达有关。     

Effects of protein tyrosine kinase inhibitors on cytokine-induced adhesion molecule expression by human umbilical vein endothelial cells.

1. Endothelial cells can be stimulated by the pro-inflammatory cytokines interleukin (IL)-1 alpha and tumour necrosis factor (TNF) alpha to express the leukocyte adhesion molecules E-selectin, vascular cell adhesion molecule (VCAM)-1 and intercellular adhesion molecule (ICAM)-1 but the intracellular signalling mechanisms leading to this expression are incompletely understood. We have investigated the role of protein tyrosine kinases (PTK) in adhesion molecule expression by cytokine-activated human umbilical vein endothelial cells (HUVEC) using the PTK inhibitors genistein and herbimycin A, and the protein tyrosine phosphatase (PTP) inhibitor sodium orthovanadate. 2. Maximal E-selectin expression induced by incubation of HUVEC for 4 h with IL-1 alpha (100 u ml-1) and TNF alpha (100 u ml-1) was dose-dependently inhibited by genistein and herbimycin A. Although similar effects were seen on phorbol 12-myristate, 13-acetate (PMA)-induced expression, this was not due to inhibition of protein kinase C (PKC) activity as the selective inhibitors of PKC, bisindolylmaleimide (BIM), Ro31-7549 or Ro31-8220 did not affect IL-1 alpha- or TNF alpha-induced E-selectin expression at concentrations which maximally inhibited PMA-induced expression. 3. Genistein inhibited VCAM-1 expression induced by incubation of HUVEC for 24 h with TNF alpha or IL-1 alpha whereas it did not affect ICAM-1 expression induced by 24 h incubation with either of these cytokines. Herbimycin A inhibited both VCAM-1 and ICAM-1 expression induced by TNF alpha. 4. Basal expression of E-selectin, VCAM-1 and ICAM-1 was dose-dependently enhanced by sodium orthovanadate. In contrast, vanadate differentially affected TNF alpha-induced expression of these molecules with maximal E-selectin and ICAM-1 expression being slightly enhanced and VCAM-1 expression dose-dependently reduced. 5. We also studied the effects of PTK and PTP inhibitors on adhesion of the human pre-myeloid cell line U937 to TNF alpha-stimulated HUVEC. Adhesion of U937 cells to HUVEC pretreated for 4 or 24 h with TNF alpha was dose-dependently inhibited by genistein and herbimycin A but unaffected by daidzein. Adhesion of U937 cells after 4 h was partially inhibited by blocking antibodies against both E-selectin and VCAM-1 but after 24 h was only inhibited by anti-VCAM-1. 6. Sodium orthovanadate had no effect on TNF alpha-induced U937 adhesion but dose-dependently enhanced adhesion to unstimulated HUVEC. Vanadate-induced adhesion was inhibited by an antibody against VCAM-1. 7. These results demonstrate that PTK-mediated phosphorylation events are important for the regulation of adhesion molecule expression by human endothelial cells, and additionally show that PTK inhibitors differentially affect upregulation of different adhesion molecules, implicating divergent regulatory pathways for cytokine-induced adhesion molecule expression.     

Protective effects of eugenol against oxidized LDL-induced cytotoxicity and adhesion molecule expression in endothelial cells.

Eugenol, a natural constituent of a number of aromatic plants and their essential oil fractions, has several biological effects. However, its protective effects against endothelial injury remain unclarified. This study investigates how eugenol affects human umbilical vein endothelial cells (HUVECs) dysfunction mediated by oxidized low density lipoprotein (oxLDL). Our results showed that the suppression of endothelial NO synthase (eNOS) expression, enhancement of adhesion molecules (ICAM, VCAM, and E-selectin) expression, and adherence of monocytic THP1 cells caused by a non-cytotoxic concentration (100 microg/ml) of oxLDL were ameliorated following a eugenol treatment (12.5-100 microM) in HUVECs. Eugneol also inhibited the reactive oxygen species (ROS) generation, intracellular calcium accumulation, and the subsequent mitochondrial membrane potential collapse, cytochrome c release and caspase-3 activation induced by oxLDL. The cytotoxicity and apoptotic features induced by a cytotoxic concentration (200 microg/ml) of oxLDL was also attenuated by eugenol. Our results suggest that eugenol may protect against the oxLDL-induced dysfunction in endothelial cells.