HRP标记AcLDL_2在AcLDL受体研究中的应用

用辣根过氧化物酶标记的ＡｃＬＤＬ２培养小白鼠腹腔巨噬细胞，直观地显示了巨噬细胞表面ＡｃＬＤＬ受体的存在，此受体只特异性的识别修饰的ＬＤＬ，其识别作用与配体分子荷大量负电荷有关。     

Inadequate dietary magnesium intake increases atherosclerotic plaque development in rabbits

Epidemiological studies have shown dietary magnesium (Mg) intake and serum Mg levels to be inversely correlated with the development of atherosclerosis. We hypothesized that low levels of Mg would promote atherosclerotic plaque development in rabbits. New Zealand white rabbits (4 months old, n = 22) were fed an atherogenic diet containing 0.12% (−Mg), 0.27% (control), or 0.43% (+Mg) Mg for 8 weeks. Blood samples were obtained at baseline, 2, 4, 6, and 8 weeks and were assayed for total cholesterol, high-density lipoprotein (HDL), non-HDL, triglycerides (TG), C-reactive protein, serum Mg, and erythrocyte Mg. Aortas from −Mg had significantly more plaque, with an intima thickness 42% greater than control and 36% greater than +Mg. Serum cholesterol levels rose over time, and at 8 weeks, −Mg had the highest and +Mg the lowest total and non-HDL cholesterol and TG levels, although these results did not reach significance. Over time, serum Mg levels increased, and erythrocyte Mg levels decreased. C-reactive protein significantly increased in all groups at 4 and 6 weeks but returned to baseline levels by 8 weeks. This study supports the hypothesis that inadequate intake of Mg results in an increase in atherosclerotic plaque development in rabbits.     

雷帕霉素对炎性反应状态下肾小球系膜细胞内脂质稳态的影响

Objective To investigate the effect of rapamycin on cholesterol homeostasis of glomerular mesangial cells and the underlying mechanism. Methods Glomerular mesangial cell line (HMCL) cells were cultured and divided into control group, IL-1β group and different concentration rapamycin groups. Intracellular cholesterol accumulation was observed and measured by oil O staining and HPLC. Real-time quantitative PCR and Western blot were used to detect the mRNA and protein expression of LDLR, PPARγ, LXRα, ABCA1 in HMCL after the treatment with IL-1β and rapamycin. Results Rapamycin had no significant influence on intracellular cholesterol concentration under normal condition. IL-1β significantly increased the intracellular cholesterol concentration by 143％ of control (P<0.05), and 10, 50, 100 ?滋g/L rapamycin could significantly inhibit the effect of IL-1β (87％, 116％, 96％ of control respectively, all P<0.05). Rapamycin could suppress the increased expression of LDLR caused by IL-1β on both mRNA and protein level in a dose-dependent manner（P<0.01）. Rapamycin dose-dependently up-regulated the reduced mRNA and protein expression of ABCA1, the decreased mRNA expression of PPARγ and LXRα induced by IL-1β as well (P<0.01）. Conclusion Rapamycin may contribute to the maintenance of intracellular cholesterol homeostasis in glomerular mesangial cells under inflammatory state by both reducing cholesterol uptake and promoting cholesterol efflux.     

Cyclic tensile stretch load and oxidized low density lipoprotein synergistically induce lectin-like oxidized ldl receptor-1 in cultured bovine chondrocytes, resulting in decreased cell viability and proteoglycan synthesis.

Mechanical stimulation is known to be an essential factor in the regulation of cartilage metabolism. We tested the hypothesis that expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) can be modulated by cyclic tensile stretch load in chondrocytes. Cyclic loading of repeated stretch stress at 10 cycles per minute with 10 kPa of stress for 6 h induced expression of LOX-1 to 2.6 times control in cultured bovine articular chondrocytes, equivalent to the addition of 10 microg/mL oxidized low density lipoprotein (ox-LDL) (2.4 times control). Application of the cyclic load to the chondrocytes along with 10 microg/mL ox-LDL resulted in synergistically increased LOX-1 expression to 6.3 times control. Individual application of cyclic loading and 10 microg/mL ox-LDL significantly suppressed chondrocytes viability (84.6% +/- 3.4% and 80.9% +/- 3.2% of control at 24 h, respectively; n = 3; p < 0.05) and proteoglycan synthesis [81.0% +/- 7.1% and 85.7% +/- 5.2% of control at 24 h, respectively; p < 0.05 when compared with 94.6% +/- 4.6% for native-LDL (n = 3)]. Cyclic loading and 10 microg/mL ox-LDL synergistically affected cell viability and proteoglycan synthesis, which were significantly suppressed to 45.6% +/- 4.9% and 48.7% +/- 6.7% of control at 24 h, respectively (n = 3; p < 0.01 when compared with individual application of cyclic loading or 10 microg/mL ox-LDL). In this study, we demonstrated synergistic effects of cyclic tensile stretch load and ox-LDL on cell viability and proteoglycan synthesis in chondrocytes, which may be mediated through enhanced expression of LOX-1 and which has important implications in the progression of cartilage degeneration in osteoarthritis.     

血清低密度脂蛋白胆固醇直接测定与Friedewald公式计算结果比较

采用聚乙烯硫酸（ＰＶＳ）沉淀法测定血清低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）值，同时应用Ｆｒｉｅｄｅｗａｌｄ公式计算ＬＤＬ－Ｃ含量，并对两法结果进行比较分析，提出当甘油三脂（ＴＧ）＜４．５２ｍｍｏｌ／Ｌ时，Ｆ公式计算法可代替ＰＶＳ法，当ＴＧ＞４．５２ｍｍｏｌ／Ｌ时，不宜用Ｆ公式计算ＬＤＬ－Ｃ的值。     

噪声和咖啡因联合作用对血液中TG、Ch、LDL和HDL含量的影响

用自动生化分析仪对接触强噪声的纺织女工饮用咖啡前后和不接触强噪声的女大学生进行了血液TG、Ch、LDL和HDL含量测定。结果发现:噪声可使血液TG、Ch及LDL含量显著升高,而噪声和咖啡(含咖啡因)联合作用后其血液TG、Ch及LDL含量明显降低,HDL含量升高,提示咖啡因可拮抗噪声所致的脂代谢异常。     

救心胶囊对LDL损伤内皮细胞抗氧化损伤能力影响的实验研究

[目的]观察救心胶囊对低密度脂蛋白(LDL)损伤后内皮细胞抗氧化损伤能力的影响,以探讨该复方保护内皮细胞和防治冠心病的作用机制。[方法]运用内皮细胞培养技术,建立LDL损伤模型,并以两种不同的给药方式——无菌中药提取液和载药血清进行分组培养,并观察内皮细胞超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量的变化。[结果]内皮细胞LDL损伤后,其SOD活性显著降低,而MDA含量明显升高,而中药处理后能有效抑制上述改变。[结论]救心胶囊能增强细胞的抗氧化损伤能力,具有良好的保护内皮细胞的作用。     

Lipoprotein lipase in relation to inflammatory activity in rheumatoid arthritis

Objective. To evaluate the impact of chronic inflammation on lipoprotein lipase (LPL) levels and triglyceride metabolism in patients with rheumatoid arthritis (RA). Design. Plasma levels of LPL activity and mass before and after heparin were determined in post-menopausal women with active RA and in controls. The results were related to lipid levels and inflammatory variables. The LPL activity and mass together with triglyceride levels were also measured before and 6 h after an oral fat load. Setting. The study was performed on in- and out-patients at a University Rheumatology clinic. The controls came from the same reference area. Subjects. Altogether 17 consecutive post-menopausal female patients with RA and 16 age and sex matched controls were enrolled for the initial determination of LPL. Fifteen of the patients and 15 of the controls agreed to take part in the fat load. Of these, one patient and one control were excluded. Main outcome measures. LPL determination: basal levels and post-heparin levels of LPL activity and mass. Correlations between LPL and blood lipids (cholesterol, triglycerides), lipoprotein levels (high density lipoprotein, HDL; low density lipoprotein, LDL), erythrocyte sedimentation rate (ESR) acute phase proteins (orosomucoid, haptoglobin, fibrinogen mass) and cytokines (tumour necrosis factor α, TNF-α; interleukin 1β, IL-1β; and interleukin-6, IL-6). Fat tolerance test: LPL activity, mass and triglyceride levels before and 6 h after a per oral fat load. Results. Pre-heparin LPL mass (P<0.01) and activity (P<0.01) were significantly lower in the rheumatoid patients. Pre-heparin LPL mass showed no correlation to the lipid levels, but an inverse correlation to several inflammatory parameters; it was significant for orosomucoid (r_s=?0.63, P<0.05) and C-reactive protein (CRP) (r_s=?0.54, P<0.05) and close to significant for haptoglobin (r_s=?0.48, P=0.087) and IL-6 (r_s=?0.52, P=0.061). Six hours after a lipid load the LPL activity and mass were significantly lower in RA (P<0.05 and P<0.01, respectively) but the triglyceride level was not significantly different compared to controls. Conclusion. An inverse relationship exists between inflammatory status and pre-heparin LPL mass. Pre-heparin LPL mass reflects mainly the inactive monomeric fraction of LPL. This has been shown to hinder the uptake of remnant lipoprotein particles through competition with lipoprotein bound dimeric LPL for the LDL receptor-related protein (LRP receptor) on hepatocytes and macrophages in culture. A decrease of the level of monomeric LPL in plasma may thus be beneficial for remnant catabolism. The same mechanism may on the other hand increase macrophage uptake of lipids. This may not affect global lipid metabolism but may be important in driving the atherosclerotic process in the vessel wall.     

食管癌、胃癌组织的低密度脂蛋白受体分析

以１２５Ⅰ－ＬＤＬ为配体对食管癌、胃癌及其相应的正常组织进行了ＬＤＬ受体水平的测定，同时分析了各组织中蛋白质、ＤＮＡ的含量，以探讨食管癌和胃癌发生与ＬＤＬ代谢之间的关系。结果显示，癌组织和正常组织的ＬＤＬ受体亲和性差异无显著性，但癌变组织的蛋白质、ＤＮＡ和ＬＤＬ受体水平均明显高于相应正常组织。癌细胞需要大量的胆固醇满足其有丝分裂，细胞通过受体升高机制使ＬＤＬＲ增多，以增加对ＬＤＬ的摄取和利用。