人血高密度脂蛋白制备新工艺

以血浆制备白蛋白 (Cohn 6法 )后所产生的 F - 1沉淀为原料 ,采用低温乙醇工艺 ,经过 3步分离纯化 ,再用截留分子量 5 0 k D的超滤膜超滤脱醇浓缩后 ,加入 (10± 1) %(g/ m l)蔗糖作保护剂进行巴斯德病毒灭活 ,制得人血高密度脂蛋白。制品经 SDS- PAGE显示 ,纯度 85 %～ 95 %,载脂蛋白 A 分子量 2 7.3k D,活性 4.0× 10 6u/ g蛋白以上 ,载脂蛋白 A 回收率在 6 0 %以上。     

人血白蛋白注射液澄明度检查的方法及意义

人血白蛋白注射液澄明度检查的方法及意义李皓，王俊平（西安市中心血站西安７１００６１）人血白蛋白注射液是经健康人血浆分离、提取、灭活病毒，供静脉输注的制剂。为了保持其生物活性，规定６０℃１０ｈ灭活病毒，不能进行高压灭菌。因此，澄明度检查（简称灯检）具有...     

人血高密度脂蛋白生物活性测定方法的研究

目的 :建立人血高密度脂蛋白 (HDL)生物活性检测法。方法 :根据受体酶联免疫检测法的原理和步骤 ,以超速离心制备的HDL为参考品 ,以每 1 μgapoAⅠ为一个HDL活性单位 ,通过HDL生物活性标准曲线双对数回归方程 ,求测待测HDL制剂的生物活性。结果 :标准曲线在 1～ 1 6个活性单位范围内呈线性关系。测定的板内及板间变异系数分别为 7.6 %～ 9.5 %及 1 2 .3%。结论 :此法操作简便 ,重复性好 ,且HDL以外的脂蛋白不干扰检测反应 ,可作为检测人血浆HDL制剂生物活性的方法。     

人血白蛋白注射液的药品评价研究进展

依据《中国药品综合评价指南参考大纲》对人血白蛋白(human serum albumin, HSA)注射液进行药品评价。查阅HSA注射液相关的诊疗指南、药典、药品说明书、文献及官方数据,对其安全性、有效性、顺应性、经济性等进行描述性分析。HSA注射液临床应用广泛且安全性好,但价格偏贵,医保仅限抢救、重症或因肝硬化、癌症引起胸腹水的患者(HSA低于30 g·L^-1);HSA注射液已被多个国家的指南推荐用于肝硬化腹水、低血容量休克等疾病的治疗,但临床仍有不合理用药的情况发生。     

对肾综合征出血热早期应用病毒唑注射液人血白蛋白及地塞米松注射液的疗效探讨

目的 本文报告应用病毒唑、白蛋白、及地塞米松注射液采用随机配对方法台疗50例肾综合征出血热，结果表明，早期应用控制病毒血症，保护血管壁，减少或避免低血压休克期，促进越期和降低病死率，疗效肯定。治疗组越过低血压休克期及少尿期为100％，对照组分别为70％和74％两组对比差异显著。我们认为及早应用病毒唑，人血白蛋白，地塞米松，尤其是发病的3—5天内治疗肾综合征出血热，对于提高治愈率，降低患者的费用效果更显著。     

人血白蛋白注射液不良反应一例

<正>患者女,57岁。于2011年7月14日因腹部胀痛3月余,加重伴呼吸困难3d,以"腹水原因待查"收治入院。入院后观察患者神志清楚,精神差,腹部膨隆,大量腹腔积液,全身水肿,双下肢水肿严重。心电监护仪测量生命体征为     

奥扎格雷钠注射液联合人血白蛋白治疗脑梗死疗效观察

我院自2000年1月至2002年8月采用奥扎格雷钠注射液联合人血白蛋白治疗急性期脑梗死62例,效果良好.报告如下.     

尼莫地平注射液的研制

目的:研制使用时无须三通阀的尼莫地平注射液。方法:采用正交实验优选处方,并测定了其与氯化钠注射液配伍10h后的含量。结果:按最优化处方配制的注射液与氯化钠注射液配伍后,在10h内尼莫地平不会析出,且稳定性良好。结论:本品使用方法符合临床习惯,应用前景良好。     

重组高密度脂蛋白-紫杉醇对结肠癌的靶向性研究

目的：制备重组高密度脂蛋白-紫杉醇复合物（γHDL-PTX）,研究其对结肠癌的靶向作用。方法：薄膜分散法制备γHDL-PTX,采用HPLC法定量考察结肠癌细胞HT-29对γHDL-PTX的摄取作用;采用MTT法测定研究γHDL-PTX对HT-29细胞的增殖抑制作用;采用HPLC法测定γHDL-PTX在荷瘤鼠中的组织分布情况;构建rHDL-DiR并采用裸鼠活体成像法观察载体在荷瘤鼠的分布情况。结果：细胞试验表明HT-29细胞对γHDL-PTX摄取高于对PTX溶液、γHDL-PTX核的摄取,IC₅₀显著低于其他两种剂型（P < 0.01）。组织分布及裸鼠活体成像试验表明γHDL-PTX在肿瘤组织的分布较其他两种剂型有所提高。结论：γHDL作为抗肿瘤药物载体对结肠癌具有较好的靶向性能,具有较为广阔的应用前景。     

辛伐他汀对实验性高脂血症小鼠高密度脂蛋白的影响

目的:探讨辛伐他汀对动脉粥样硬化(As)形成过程中高密度脂蛋白(HDL)性质及其相关酶活性的影响。方法:喂食高脂饲料建立C57BL/6小鼠高脂血症模型,利用辛伐他汀(20mg.kg-1)给予小鼠灌胃8周,血浆经快速蛋白液相色谱(FPLC)分离后酶法检测各脂蛋白的胆固醇水平,酶法测定HDL相关抗氧化酶对氧磷酯酶1(PON1)和血小板活化因子-乙酰水解酶(PAF-AH)活性。结果:辛伐他汀使C57BL/6高脂模型鼠血清总胆固醇水平降低了34.4%,甘油三酯水平下降60.2%,HDL-C水平仅增高7.8%,但HDL相关的PON1和PAF-AH酶活性明显升高。结论:辛伐他汀不仅能显著改善血脂水平,同时能有效增强HDL的抗氧化能力,表现出较强的抗As作用。     

血脂康对高血压患者高密度脂蛋白胆固醇水平的影响

目的观察血脂康对高血压患者高密度脂蛋白胆固醇(HDL-C)水平的影响。方法 90例高血压患者随机分为试验组与对照组,在常规治疗的基础上,试验组给予血脂康胶囊600 mg,2次/d;对照组给予安慰剂2粒,2次/d。治疗6个月后观察疗效,测定用药前和用药6个月后血浆HDL-C水平变化。将试验组受试者按基线HDL-C水平由低到高分为A组(HDL-C<1.0 mmol/L),B组(1.0 mmol/L≤HDL-C<1.5 mmol/L),C组(HDL-C≥1.5 mmol/L),治疗6个月后血脂康升高HDL-C的幅度。结果治疗6个月后,试验组HDL-C水平较用药前升高(P<0.05),且治疗后试验组HDL-C水平高于对照组(P<0.05)。治疗6个月后血脂康升高HDL-C的幅度在A、B、C 3组分别为基线水平的23.7%、10.8%、0.04%。结论血脂康可显著升高高血压患者HDL-C水平,随着HDL-C基线水平的逐步升高,血脂康升高HDL-C的幅度越来越低。     

Impact of short‐term low‐dose atorvastatin on low‐density lipoprotein and high‐density lipoprotein subfraction phenotype

Statins can significantly reduce low‐density lipoprotein–cholesterol (LDL‐C) and modestly raise or not alter high‐density lipoprotein–cholesterol (HDL‐C). However, their impact on high‐density lipoprotein (HDL) and low‐density lipoprotein (LDL) subfractions has been less examined. The aim of the present study was to investigate the short‐term impact of low‐dose atorvastatin on HDL and LDL subfractions in humans. In this randomized study, data from 52 subjects were analysed. Thirty‐seven patients with atherosclerosis were randomized to treatment with atorvastatin 10 mg/day (n = 17) or 20 mg/day (n = 20) for 8 weeks, with 15 healthy subjects without therapy used as a control group. The lipid profile and lipoprotein subfractions were determined using the Lipoprint system at baseline and at 8 weeks. The data suggest that atorvastatin treatment (10 and 20 mg/day) for 8 weeks significantly decreases LDL‐C levels and reduces the cholesterol concentration of all LDL subfractions, which is accompanied by an increase of the mean LDL particle size. Although 10 mg/day atorvastatin treatment for 8 weeks had no impact on the HDL subfraction, 20 mg/day atorvastatin for 8 weeks significantly increased the cholesterol concentration of large HDL particles and decreased the cholesterol concentration of small HDL particles without changing serum HDL‐C levels in patients with atherosclerosis. Therefore, the results suggest that 20 mg/day atorvastatin treatment for 8 weeks may result in a favourable modification of the HDL subfraction phenotype in addition to its effects on the cholesterol concentration of all LDL subfractions and mean LDL particle size.     

高密度脂蛋白胆固醇酯化速率与冠心病的相关性

【摘要】目的探讨高密度脂蛋白胆固醇酯化率（FERnDL）与冠心病的相关性。方法按冠状动脉造影结果将120例研究对象分为冠心病组（n=60）和非冠心病组（n=60）,进行临床数据收集。对FER吼进行测定,分析FER HDL与冠心病的相关性。结果冠心病组FERHDL[（21．70±8．73）％／h]显著高于非冠心病组[（18．65±6．26）％／h、（P〈0．05）,且FER-随病变支数增加而逐渐增高（P〈0．05）。结论冠心病患者的FERHDL显著高于非冠心病患者,并且冠心病越严重FER眦越高,呈现明显的正相关。     

Activation of membrane outward currents by human low density lipoprotein in mouse peritoneal macrophages

Summary The aim of the present study was to search for electrophysiological effects of human lipoproteins on membrane currents in mouse peritoneal macrophages which had been cultured for 5 to 20 days. Whole-cell currents were recorded by using a voltage-clamp technique.Low density lipoprotein (LDL, 100 g/ml) increased a slowly activating nonspecific cation current (i_so) in the positive potential range to 244 ± 23% of the reference (test potential + 55 mV, n = 13, P < 0.005). Augmentation of current resulted out of a negative shift of the activation curve along the voltage axis (–22 mV) and an increase of maximally available current.Furthermore, LDL increased a rapidly activating outward current (i_fo) at test potentials positive to the potassium equilibrium potential. At +55 mV i_fo-amplitude increasedto 165 ± 14% ofreference (n = 16, P < 0.005). LDL-induced effects on i_fo-current could be mimicked by application of the calcium ionophore A 23187 (1 mol/l) which led to an increase of i_fo-current to 161 ± 25% of the reference (test potential + 55 mV, n = 11, P < 0.005).Acetylated-LDL (100 g/ml, 5–15 min) produced no significant effect on the membrane currents under investigation. Correspondence to U. Borchard at the above address     

High‐density lipoprotein: A potent inhibitor of inflammation

1. Inflammation is an important process, driving the progression of atherosclerosis. Stemming inflammation may be a mechanism to inhibit the progression of this disease. 2. High‐density lipoprotein (HDL), a particle inversely related to cardiovascular disease, has been described as having a number of anti‐inflammatory functions. It has been shown that HDL inhibits endothelial inflammation in both in vitro and in vivo models, reducing the expression of key cell adhesion molecules. In addition, HDL has been shown to have an effect on the coagulation pathway by inhibiting platelet activation and reducing thrombus formation. Furthermore, by reducing the activation of leucocytes, HDL can inhibit leucocyte recruitment to the endothelium. 3. High‐density lipoprotein infusion studies conducted in patients with inflammatory diseases have shown that acute treatment with HDL can effectively inhibit inflammation in vivo. Thus, HDL has been proven to be a potent inhibitor of inflammation, acting on a number of pathways, and this may suggest that HDL could be applied as an anti‐inflammatory molecule for a number of diseases. 4. The present review highlights these important studies and reviews data on the anti‐inflammatory effects of HDL from in vitro and in vivo studies, in both humans and animal models of atherosclerosis and inflammatory‐related diseases.     

高密度脂蛋白与载脂蛋白A1、低密度脂蛋白与载脂蛋白B的相关性分析

目的对高密度脂蛋白与载脂蛋白A1、低密度脂蛋白与载脂蛋白B之间的相关性进行分析探讨。方法随机抽取在2010年1月～2012年5月间在本院进行体检的500名受检者,对其进行血清高密度脂蛋白(HDL-C)、低密度脂蛋白(LDL-C)、载脂蛋白A1(apoA1)、载脂蛋白B(apoB)测定,并按照三酰甘油(TG)水平的不同进行分组,分析HDL-C与apoA1、LDL-C与apoB之间的相关性。结果在TG水平小于10.00mmol/L时,HDL-C与apoA1、LDL-C与apoB之间存在明显的相关性,在TG水平大于10.00mmol/L时,HDL-C与apoA1、LDL-C与apoB不具有明显的相关性。结论在一定条件下,HDL-C与apoA1、LDL-C与apoB存在比较明显的相关性,这将对临床诊断与治疗评价产生重要意义,值得关注。     

Synthetic nano-low density lipoprotein as targeted drug delivery vehicle for glioblastoma multiforme

The low density lipoprotein (LDL) receptor has been shown to be upregulated in GBM tumor cells and is therefore a potential molecular target for the delivery of therapeutic agents. A synthetic nano-LDL (nLDL) particle was developed and tested to determine its utility as a drug delivery vehicle targeted to GBM tumors. nLDL particles were constructed by combining a synthetic peptide containing a lipid binding motif and the LDL receptor (LDLR) binding domain of apolipoprotein B-100 with a lipid emulsion consisting of phosphatidyl choline, triolein, and cholesteryl oleate. Composition analysis, fast protein liquid chromatography, and electron microscopy revealed that nLDL was highly reproducible and intermediate in size between high density lipoprotein and LDL particles (10.5+/-2.8 nm diameter). The binding and uptake of fluorescently labeled nLDL particles was assessed using fluorescence microscopy. Uptake of nLDL was time dependent, exhibiting saturation at approximately 3 h, and concentration dependent, exhibiting saturation at concentrations greater than 5 microM peptide. Using Lysotracker as a cellular marker, nLDL co-localized with lysosomes. nLDL binding was eliminated by blocking LDLRs with suramin and nLDL inhibited binding of plasma LDL to LDLRs. Collectively these data strongly suggest that the synthetic nano-LDLs described here are taken up by LDLR and can serve as a drug delivery vehicle for targeting GBM tumors via the LDLR.     

氯沙坦对冠心病患者血浆氧化修饰低密度脂蛋白的影响

目的 :观察氯沙坦对冠心病患者血浆氧化修饰低密度脂蛋白 (ox LDL)的影响。方法 :选择确诊冠心病患者 30例以及年龄、性别相匹配的健康志愿者 30例。冠心病组予氯沙坦 (5 0± 15 )mg·d-1× 3mo,于治疗前后分别采集清晨空腹血 ,以检测ox LDL、丙二醛 (MDA)含量。结果 :治疗前冠心病组ox LDL、MDA水平显著高于对照组 ,分别为P <0 0 5和P <0 0 1。氯沙坦治疗 3mo后冠心病组ox LDL与MDA含量较用药前显著降低 ,分别为P <0 0 5和P <0 0 1。结论 :氯沙坦可以降低冠心病患者血浆ox LDL与MDA水平