黄芪治疗原发性肾病综合征的疗效观察

目的 :探讨黄芪治疗原发性肾病综合征的疗效。方法 :将 97例肾病综合征患者随机分三组 ,泼尼松组 (对照组 )、丹参组 (泼尼松 +丹参 )、黄芪组 (泼尼松 +黄芪 ) ,观察三组患者治疗前后尿蛋白、血清白蛋白、血脂变化及症状、体征改善情况。结果 :三组治疗后均见尿蛋白减少、血清白蛋白升高和总胆固醇下降 (P <0 .0 1) ,但黄芪组与丹参组和对照组相比 ,黄芪组在使尿蛋白减少、血清白蛋白升高和总胆固醇下降方面尤为明显 (P <0 .0 1) ;黄芪组在水肿消退、腹胀改善方面明显好于丹参组及对照组 (P <0 .0 5 )。结论 :黄芪能减少原发性肾病综合征患者的尿蛋白排泄 ,提高血清白蛋白 ,降低血脂水平及改善相应的临床症状。     

双诺希胶囊对实验性高脂血症的影响

目的　验证双诺希胶囊 ( SHNX)对高脂血症大鼠血脂的影响 .方法　用高脂饲料喂饲大鼠建立高脂血症模型 ;随机分为 6组 ,即正常对照组、高脂模型组、SHNX大剂量组( SHNXH1.2 0 0 g· kg- 1 )、SHNX中剂量组 ( SHNXM0 .60 0 g· kg- 1 )、SHNX小剂量组 ( SHNXL 0 .3 0 0 g· kg- 1 )和安妥明组 ( Clofibrate) ,连续喂饲并灌胃给药 3 0 d后 ,观察 SHNX对高脂血症大鼠血脂含量的影响 .结果　 SHNX能明显降低血清总胆固醇 ( TC)、三酰甘油 ( TG)含量 ,亦能明显提高血清高密度脂蛋白亚组分 胆固醇 ( HDL2 - C)及高密度脂蛋白胆固醇 ( HDL - C)的含量 .结论　 SHNX对血脂紊乱大鼠有明显的治疗效果 .     

河南汉族人群载脂蛋白E基因型与血脂水平的关系

目的：研究河南汉族人群中载脂蛋白E(ApoE)基因型和等位基因频率以及ApoE表型与血脂水平之间的关系。方法：运用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法检测了317例健康人的ApoE基因型,按标准酶法和免疫学方法测定血脂和载脂蛋白。结果：研究对象的ε2,ε3和ε4等位基因频率分别为0.068、0.869和0.063,与中国其他地区汉族人群比较差异无显著性。携带ε4等位基因的个体具有较高的TC及LDL-C水平。通过人种间比较发现ε4等位基因频率在白种人群中较高。结论：黄种人群ε4等位基因频率较白种人低;ApoE基因多态性影响血中胆固醇水平。     

磷脂对HDL3介导大鼠皮肤成纤维细胞内胆固醇流出能力的影响

目的　研讨磷脂对HDL3 介导大鼠皮肤成纤维细胞内胆固醇流出能力的影响。方法　在卵磷脂 (PC)或鞘磷脂 (SPM )存在条件下 ,观察HDL3 介导细胞胆固醇流出量的变化、细胞内磷脂含量变化及游离胆固醇 /胆固醇酯平衡的变化。结果　①BSA组 (对照组 )、HDL3 组、PC组、SPM组、PC HDL3 组和SPM HDL3 组分别介导 4.70 %、31.5 5 %、7.35 %、8.0 6 %、42 .95 %和 46 .98%细胞胆固醇流出 ;②BSA、HDL3 、HDL3 SPM和HDL3 PC组细胞培育后胞内卵磷脂磷含量 (PC p)和鞘磷脂磷含量 (SPM p)分别为 2 0 .0 2、5 .5 6 ,17.5 6、5 .2 8,18.6 2、7.0 0和 2 2 .5 0、5 .5 2 μg/皿 ;③PC和SPM与细胞培育后 ,胞内游离胆固醇 /总胆固醇比值分别为 49.6 5和 5 9.5 7。培育前此比值为 48.6 4。结论　①PC和SPM本身无介导细胞胆固醇流出能力 ,但它们能显著提高HDL3 介导的细胞胆固醇流出能力 ,且后者强于前者 ;②随着细胞胆固醇流出 ,部分胞内PC也流出胞外 ,而胞内SPM无明显变化 ;③SPM促进细胞内胆固醇酯向游离胆固醇转化。     

高密度脂蛋白介导大鼠皮肤成纤维细胞内胆固醇流出的机制

目的研究高密度脂蛋白-3(HDL3)介导大鼠皮肤成纤维细胞胆固醇(ch)流出机制。方法用N-乙酰咪唑修饰HDL,阻断HDL与细胞受体相互作用,观察其对HDL3介导细胞ch流出的影响。用FITC标记HDL示踪HDL3在介导细胞ch流出中自身代谢过程。结果牛血清白蛋白(对照组)介导4.74%细胞ch流出,HDL3组和N-乙酰咪唑HDL组分别为31.85%和8.41%。FITC-HDL3与细胞37-℃培养3h后,细胞内吞荧光强度(FS)占细胞结合FS的65.78%,其中93.5%FS存在于TCA可沉淀部分。细胞进一步37-     

LDL-C直接测定法在生化分析仪上的应用

用日本第一化学药品株式会社LDL—C试剂盒在BeckmanCX4型自动生化分析仪上直接测定血清LDL—C含量。方法批内CV 0 37%～ 1 11% ,批间CV为 2 11%～ 3 0 2 % (n =2 0 )。平均回收率为 98 9% ,在 8 10mmol/L浓度范围内呈良好线性关系。TG <5 0 0mmol/L时与聚乙烯硫酸沉淀法 (X1)及Friedewald(X2 )公式计算结果相关良好 ,回归方程分别为Y =0 988X1+0 0 47,r=0 95 1,Y =0 96 1X2 +0 0 5 2 ,r=0 930。LDL—C直接测定法简单、快速 ,用血量少 ,勿需沉淀分离 ,适宜于自动化分析。     

缺铁与胆囊结石形成关系的研究

本文检测了 110例 (男 32 ,女 78)胆囊结石病人的血清铁水平 ,低于正常值者 31例 ,占 2 8 2 % ;其中女性 2 5例 ,占80 6 % ,男性仅 6例 ,占 19 4%。铁在肝脏的酶代射过程中扮演着重要角色 ,因此 ,缺铁可能改变胆固醇的代谢 ,增强胆囊结石的形成。     

高密度脂蛋白与冠心病的关系研究进展

流行病学调查、实验研究和临床观察发现,血浆高密度脂蛋白胆固醇作为一个独立的预测因素与冠心病的发病率呈负相关,HDL促进循环中的胆固醇向肝脏转运即“逆向胆固醇转运”,HDL中的两种酶－二乙基对硝基苯磷酸酯酶和血小板激活因子酰水解酶能够降低氧化HDL的形成;通过戒烟、降低到理想体重、规律的需氧锻炼、药物治疗,能绝对或相对的升高HDL－c浓度,降低冠心病的发病率。     

High affinity of sigma1-binding sites for sterol isomerization inhibitors: evidence for a pharmacological relationship with the yeast sterol C8–C7 isomerase

1. The sigma-drug binding site of guinea-pig liver is carried by a protein which shares significant amino acid sequence similarities with the yeast sterol C₈–C₇ isomerase (ERG2 protein). Pharmacologically - but not structurally - the sigma₁-site is also related to the emopamil binding protein, the mammalian sterol C₈–C₇ isomerase. We therefore investigated if sterol C₈–C₇ isomerase inhibitors are high affinity ligands for the (+)-[³H]-pentazocine labelled sigma₁-binding site.
2. Among the compounds which bound with high affinity to native hepatic and cerebral as well as to yeast expressed sigma₁-binding sites were the agricultural fungicide fenpropimorph (K_i 0.005 nM), the antihypocholesterinaemic drugs triparanol (K_i 7.0 nM), AY-9944 (K_i 0.46 nM) and MDL28,815 (K_i 0.16 nM), the enantiomers of the ovulation inducer clomiphene (K_i 5.5 and 12 nM, respectively) and the antioestrogene tamoxifen (K_i 26 nM).
3. Except for tamoxifen these affinities are essentially identical with those for the [³H]-ifenprodil labelled sterol C₈–C₇ isomerase of S. cerevisiae. This demonstrates that sigma₁-binding protein and yeast isomerase are not only structurally but also pharmacologically related. Because of its affiliations with yeast and mammalian sterol isomerases we propose that the sigma₁-binding site is localized on a sterol isomerase related protein, involved in postsqualene sterol biosynthesis.

     

Low serum cholesterol increases the risk of noncardiovascular events: An antagonist viewpoint

Summary Considerable debate concerning the apparent association of low serum cholesterol levels with enhanced noncardiovascular disease mortality has been aired in both scientific and lay publications within the past year. This debate has resulted in some medical experts calling for a moratorium on efforts to reduce serum cholesterol, particularly with drugs, and for a more conservative approach to screening and modifying cholesterol levels for the primary prevention of coronary heart disease (CHD). Observational studies, including the Framingham Heart Study, the Multiple Risk Factor Intervention Trial, the Whitehall Study, and the International Collaborative Group, have not substantiated a cause and effect relationship between naturally occurring low serum cholesterol and noncardiovascular disease mortality, such as cancer. Intervention trials designed to lower high serum cholesterol levels by diet and drugs have also not been conclusively shown to produce excess harm that offsets the benefit of reduced CHD events. Several primary and secondary CHD prevention trials, with sufficient numbers of subjects to provide the statistical power to detect potential detrimental effects of lowering cholesterol levels, are currently in progress and will be very helpful in resolving the concern about noncardiovascular disease mortality.