国产苯扎贝特与氟伐他汀联合治疗混合型高脂血症的疗效与安全性

目的 研究联合应用国产苯扎贝特与氟伐他汀治疗混合型高脂血症的安全性反有效性.方法 选取180例混合性高脂血症患者随机分为两组,单药氟伐他汀组90例,给予氟伐他汀40mg,每晚1次,用药24周;联合治疗组90例,给予氟伐他汀40 mg,每晚1次,苯扎贝特200 mg,每日2次.观察24周.结果 两组均能使患者低密度脂蛋白胆固醇水平较治疗前降低,差异有统计学意义(均P<0.01),联合治疗组能够使患者甘油三酯下降,高密度脂蛋白胆固醇升高,差异亦有统计学意义(均P<0.05).结论 联合应用氟伐他汀40 mg+苯扎贝特400 mg治疗混合型高脂血症优于单用氟伐他汀治疗,并有良好的安全性.     

血脂水平在长时期内的生物学变异

目的：探讨我国人血脂水平的长期个体内生物学变异情况。方法：在多年从事血脂标准化研究及参加国际血脂标准化计划基础上长期测定一相对稳定人群的血脂水平，分析其中23例1年多次及100例10-15年间每年1次血脂测定结果。结果：两组病例血脂水平的个体内总变异（包括生物学变异和分析变异）大致为，总胆固醇10％，甘油三酯28％，低密度脂蛋白胆固醇18％，高密度脂蛋白胆固醇16％。结论：血脂指标，尤其是甘油三酯有较大生物学变异，临床上判断血脂水平高低时需考虑到生物学变异的存在，并采取适当措施减小生物学变异。     

影响急性大动脉粥样硬化性脑梗死患者脑微出血严重程度的危险因素分析

目的探讨影响急性大动脉粥样硬化性脑梗死患者脑微出血(CMBs)严重程度的危险因素。方法收集2013年7月-2015年1月南京医科大学附属南京医院神经内科住院的TOAST分型为大动脉粥样硬化性的急性脑梗死患者112例,经磁共振磁敏感加权成像(SWI)证实有CMBs的患者56例。根据SWI上CMBs的病灶数,分为1级组9例,2级组28例,3级组19例。收集各组患者病史、一般临床资料、血生化结果及头部MRI,对两组资料进行单因素分析和相关性分析。结果单因素分析结果显示,脑微出血严重程度随着甘油三酯水平的增高而降低,随着同型半胱氨酸水平的增高而增高,随着尿酸水平的增高而增高,随着深部白质高信号Fazekas’s分级的增高而增高,3组间差异有统计学意义(P0.05)。Spearman秩相关分析显示,脑微出血严重程度与甘油三酯水平呈负相关(r=-0.443,P=0.001);与尿酸水平、同型半胱氨酸水平及深部白质高信号Fazekas’s分级呈正相关(r=0.325,P=0.015;r=0.491,P=0.001;r=0.334,P=0.009)。结论甘油三酯、尿酸、同型半胱氨酸水平及深部白质高信号Fazekas’s分级与急性大动脉粥样硬化性脑梗死患者CMBs的严重程度相关。     

保肝降脂饮对脂肪肝大鼠护肝作用的实验研究

目的探讨保肝降脂饮治疗脂肪肝的药学机制。方法采用高脂饮食诱导大鼠脂肪肝模型,实验分组为脂肪肝模型组、保肝降脂饮大、中、小剂量组、东宝肝泰对照组和正常对照组共6组。观察大、中、小剂量保肝降脂饮和东宝肝泰对大鼠血清中胆固醇(TC)、甘油三酯(TG)的含量和肝组织的超氧化物歧化酶(SOD)活性的影响,以及肝组织形态学的变化。结果模型组大鼠血清中TC、TG明显高于正常组和各治疗组(P<005),而其SOD的活性较正常组和各治疗组明显降低。肝组织切片脂滴明显堆积,正常组没有脂滴堆积,各治疗组肝组织切片显示脂滴堆积较模型组轻。结论保肝降脂饮可显著降低脂肪肝大鼠血清TC、TG含量,减轻肝细胞脂滴堆积,提高肝组织SOD活性,从而发挥降脂保肝的作用。     

高甘油三酯血症与2型糖尿病的相关性分析

目的探讨高甘油三酯血症与2型糖尿病的相关性。方法对252例合并高甘油三酯血症的2型糖尿病（T2DM）患者的糖化血红蛋白（HbA1C）、甘油三酯（TG）、胆固醇（TC）、高密度脂蛋白-胆固醇（HDL-C）、低密度脂蛋白-胆固醇（LDL-C）做回顾性分析。根据NCEP-ATPⅢ将TG分为：正常水平〈1.7mmol/L,边缘性升高1.7～2.2mmol/L,高2.2～5.6mmol/L,很高≥5.6mmol/L。结果所有血脂中甘油三酯升高与2型糖尿病的相关性最强。结论甘油三酯水平增高是2型糖尿病相关的独立危险因素。血糖控制越差,甘油三酯水平越高。     

雷诺嗪对高脂高糖诱导的胰岛β细胞NIT-1功能损伤的保护作用

目的 观察雷诺嗪对高糖高脂诱导的胰岛β细胞NIT-1三酰甘油(TG)含量及脂肪酸转位酶(FAT/CD36)表达的增加和胰岛素分泌功能损伤的保护作用. 方法 用放免法检测高糖高脂及5 μmol.L^-1雷诺嗪共同作用后细胞基础胰岛素分泌(BIS)和葡萄糖刺激后胰岛素分泌(GSIS)水平的变化,酶法检测胞内TG含量,Western blot检测细胞FAT/CD36蛋白的表达. 结果正常组、高糖高脂组和雷诺嗪组的胞内TG含量分别为(2.31±0.05),(5.17±0.03)和(3.63±0.01) mmol.L^-1;BIS分别为(0.67±0.03),(0.32±0.07),(0.51±0.03)ng.mL^-1,GSIS分别为(1.68±0.17),(1.35±0.08),(1.47±0.11)ng.mL-1;FAT/CD36的相对表达量比值A1分别为(0.53±0.08),(1.78±0.05)和(1.07±0.06). 与正常组比较,高糖高脂组GSIS降低,细胞内TG含量增多. FAT/CD36蛋白表达显著增加(P<0.05). 而雷诺嗪与高糖高脂的共同作用24 h后可以显著升高GSIS,同时降低胞内TG含量,减少FAT/CD36蛋白. 结论 雷诺嗪对高糖高脂导致的胰岛细胞NIT-1分泌功能损伤有保护作用,同时可以减少胞内脂质沉积,其分子机制可能是通过脂肪酸转位酶FAT/CD36蛋白表达的改变.     

益气化浊胶囊对自发性2型糖尿病KKAy小鼠TG和TC的影响

目的观察中药益气化浊胶囊对自发性2型糖尿病KKAy小鼠血清三酰甘油和胆固醇的影响。方法以发病周龄的KKAy小鼠为研究对象,加高脂饲料制备2型糖尿病模型,经灌胃10周后,血糖仪试纸法测空腹血糖(FBG),使用酶法测血清三酰甘油(TG)和胆固醇(TC)的含量。结果益气化浊胶囊高剂量组能很好地降低血清三酰甘油的水平(P<0.01),高剂量与吡格列酮组疗效相当,低剂量效果不明显;益气化浊胶囊高、低剂量组与吡格列酮组,对血清总胆固醇无明显降低作用。结论益气化浊胶囊可降低KKAy小鼠血清三酰甘油水平,有助于降低血糖。     

Recombinant C3adesArg/acylation stimulating protein (ASP) is highly bioactive: A critical evaluation of C5L2 binding and 3T3-L1 adipocyte activation

C5L2 is a recently identified receptor for C5a/C5adesArg, C3a and C3adesArg (ASP). C5a/C5adesArg bind with high affinity, with no identified activation. By contrast, some studies demonstrate C3a/ASP binding/activation to C5L2; others do not. Our aim is to critically evaluate ASP/C3adesArg-C5L2 binding and bioactivity.Cell-associated fluorescent-ASP (Fl-ASP) binding to C5L2 increased from transiently transfected < stably transfected < Fl-ASP-sorted C5L2-HEK for both human C5L2 and mouse C5L2. Transfected C5L2-CHO cells had similar results. Endogenous C5L2 expression increased from 3T3-L1 preadipocytes < 3T3-L1 adipocytes < primary mouse adipocytes. Non-transfected cells ± Fl-ASP demonstrated background fluorescence only.In adherent C5L2-HEK (Fl-ASP sorted) and 3T3-L1 cells, blocking with 10% fetal calf serum, protamine sulfate or ovalbumin prevented ¹²⁵I-ASP non-specific binding (NSB, no cells), while albumin increased NSB. Binding to non-transfected HEK was comparable to NSB. Optimal specific binding was obtained at 20 °C (vs. 4 °C) in PBS or serum-free medium with K_d 83.7 ± 23.7 nM (C5L2-HEK), 66 ± 15 nM (C5L2-CHO) and 76 ± 14.3 nM (3T3-L1 preadipocytes); ¹²⁵I-C5a binding had greater affinity. Fl-ASP-C5L2 binding was comparable and concentration dependent (K_d 31 nM (direct binding) and IC₅₀ 35 nM (competition binding) regardless of conditions).Recombinant ASP (rASP) produced in modified Escherichia coli Origami (DE3) (allowing folding and disulphide bridge formation), purified under non-denaturing conditions demonstrated 10× greater bioactivity vs. proteolytically derived plasma ASP for triglyceride synthesis and fatty acid uptake in 3T3-L1 adipocytes and preadipocytes while adipose tissue from C5L2 KO mice was non-responsive. rASP stimulation of adipocyte BODIPY-fatty acid uptake demonstrated EC₅₀ 115 ± 93 nM and maximal stimulation of 413 ± 33%, p < 0.001. ASP binding has distinct characteristics that lead to C5L2 activation and increased bioactivity.     

Serum and hepatic lipid levels in rats infected with Trypanosoma brucei

Trypanosoma brucei, Federe strain, caused an acute infection in rats after intraperitoneal inoculation of 10⁶ trypanosomes. Parasitemia occurred from day 3 post-infection (pi) with peak parasitemia from day 7 pi. Anemia was observed between days 7 and 11 pi. The serum triglyceride concentration was comparable with the control value on day 7 pi, but increased (P < 0.05) above the control value on day 11 pi. The serum total cholesterol, high density lipoprotein (HDL), and low density lipoproteins (LDL) cholesterol concentrations decreased (P < 0.0.05) when compared with the control values on days 7 and 11 pi. The LDL cholesterol decreased more on day 11 than day 7 pi. The liver content of triglycerides and total cholesterol decreased (P < 0.05) during the infection from control values on days 7 and 11 pi. The decrease in hepatic triglyceride concentration was more on day 11 than day 7 pi, while the hepatic total cholesterol content decreased to comparable extents on days 7 and 11 pi. Hepatic LDL cholesterol content was unaffected on day 7 pi, but decreased (P < 0.05) on day 11 pi. The content of HDL cholesterol in the liver did not vary (P > 0.05) significantly during the infection. It was concluded that the decreased hepatic contents of these lipids were consistent with the serum lipid concentration, which did not seem to favor lipid uptake by hepatocytes.