Relationship Between Blood Lipid Level and In-hospital Death in Patients With Aortic Dissection / 中国循环杂志

Objective: To investigate the relationship between blood lipid level and in-hospital death in patients with aortic dissection (AD). Methods: Our retrospective study included in 2 groups: AD group, n=153 patients which was further divided into 2 subgroups:Thoracic AD subgroup, n=73 and Abdominal AD subgroup, n=80; Control group, n=50 patients with isolated hypertension at the same period. Blood lipid levels were compared among different groups and subgroups; HDL-C levels were studied by correlation analysis between AD survivor and in-hospital died AD patients. Results: Compared with Control group, AD group had increased TC [3.89 (3.19, 4.61) mmol/L] vs [3.58 (2.70, 4.33) mmol/L], decreased HDL-C [1.02 (0.86, 1.25) mmol/L vs 1.52 (1.22, 1.76) mmol/L] and lower ratio of HDL-C/TC [0.28 (0.22, 0.34) vs 0.45 (0.31, 0.67)], all P<0.01. Compared with Abdominal AD subgroup, Thoracic AD subgroup had the lower ratio of HDL-C/TC [0.27 (0.20, 0.33) vs 0.30 (0.24, 0.36)], P<0.05. Compared with AD survivor, the in-hospital died AD patients had the lower HDL-C level [0.82 (0.69, 1.04) mmol/L vs 1.06 (0.89, 1.33) mmol/L], P<0.01. Spearman correlation analysis revealed that HDL-C level was negatively related to in-hospital death of AD (correlation coefficient =-0.353). Conclusion: AD patients had abnormal lipid metabolism, blood HDL-C level was negatively related to in-hospital death in AD patients.

Neferine protects endothelial cells against damages induced by LPC and relationship with asymmetric dimethylarginine / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the protective effect of neferine against damages of endothelial cells induced by lysophos-phatidylcholine (LPC) and the relationship with asymmetric dimethylarginine (ADMA).</p><p><b>METHOD</b>The human umbilical vein endothelial cells (HUVEC-12) were treated with LPC (10 mg x L(-1)) for 24 h to establish the model of endothelial cells damages; HUVECs were prior exposed to neferine (0.1, 1.0 or 10.0 micromol x L(-1) ) for 1 h, and then exposed to LPC in the presence of the neferine for 24 h. At the end of the experiment, the cultured medium was collected for measuring the concentration of nitric oxide (NO), aleic dialdehyde (MDA) as well as ADMA and the cells were collected for measuring the level of intracellular reactive oxygen species (ROS).</p><p><b>RESULT</b>Compared with control group, exposure of endothelial cells to LPC (10 mg x L(-1)) for 24 h significantly increased the concentration of MDA and ADMA in the medium and the level of intracellular ROS and coinstantaneously significantly decreased the concentration of NO in the medium. Neferine (0.1, 1.0 or 10.0 micromol x L(-1)) significantly inhibited the elevated concentration of MDA, ADMA as well as the level of intracellular ROS and coinstantaneously significantly attenuated the decreased level of NO induced by LPC.</p><p><b>CONCLUSION</b>Neferine can protect the endothelial cells against damages induced by LPC and the protective effect is related to the decrease of the concentration of ADMA.</p>

Effects of insulin like growth factor-1 on cell viability and tissue factor in vascular endothelial cells / 中华血液学杂志

<p><b>OBJECTIVE</b>To study the effects of insulin like growth factor-1 (IGF-1) on cell viability and tissue factor (TF) in angiotensin II (Ang II) induced vascular endothelial cells and to investigate its mechanisms.</p><p><b>METHODS</b>10(-6) mol/L Ang II was added to human vascular endothelial cells (HUVECs) culture media alone or 30 min after pretreatment with IGF-1 (0.1 microg/ml , 0.5 microg/ml, 2.5 microg/ml). Cell viability and AngII type 1 receptor (AT1-R) mRNA were evaluated after 24 h incubation with AngII. At the optimum concentration of IGF-1 affecting cell viability, the time dependent manner for 12 - 48 h incubation with Ang II was evaluated. TF, NOS and NO were investigated after 24 h incubation with Ang II. In addition, NO synthase inhibitor Nomega-nitro-1-arginine methylester(L-NAME) was added 30 min before addition of IGF-1 and Ang II, and cell viability, TF, AT1-R mRNA, NOS and NO were evaluated after 24 h incubation.</p><p><b>RESULTS</b>(1) Ang II induced a decrease in cell vitality, an upregulation of AT1-R mRNA, an increase in TF, and a decrease in the activity of NOS and content of NO. (2) Pretreatment with IGF-1 significantly inhibited the decreased cell viability and upregulation of AT1-R mRNA. IGF-1 at 0.5 microg/ml showed the most obvious effects. This effect of cell viability recovery was in a time dependent manner during 12 -48 h. (3) IGF-1 also inhibited the increased content of TF, the decreased activity of NOS and the decreased content of NO. (4) The beneficial effects of IGF-1 on cultured endothelial cells were completely abolished by L-NAME.</p><p><b>CONCLUSION</b>IGF-1 pretreatment could enhance the ang II injured cell viability and anti-thrombosis capacity, and the protective effects may be related to activation of NOS-NO signaling pathway which inhibited AT1-R.</p>

Effects of Tongxinluo on cell viability and tissue factor in AngII induced vascular endothelial cells / 中南大学学报(医学版)

OBJECTIVE@#To determine the effects of Tongxinluo on cell viability and tissue factor (TF) in AngII induced vascular endothelial cells and to investigate its mechanism.@*METHODS@#AngII(10(-6)mol/L) was added to human vascular endothelial cells (HUVECs) culture media alone or with various concentration of Tongxinluo drug containing plasma (5%,10%, and 20%) added 30 minutes before AngII. Cell viability was evaluated after 24-hour incubation with AngII in a dose manner. TF, AngII type 1 receptor (AT(1)) mRNA, NO synthase (NOS) and NO were observed after 24-hour incubation with AngII. In addition, NOS inhibitor nomega-nitro-larginine (L-NAME) was added 30 minutes before Tongxinluo and AngII. Cell viability, TF, AT(1)mRNA, the level of NOS and NO were evaluated after 24-hour incubation with Tongxinluo and AngII.@*RESULTS@#Tongxinluo significantly improved AngII induced endothelial cell viability and the effect was the most obvious at 10%. Tongxinluo (10%) decreased the TF and AT(1) mRNA while increased the NOS and NO levels. L-NAME obviously inhibited the effects of Tongxinluo on cell viability, TF, AT(1) mRNA, and NOS and NO levels.@*CONCLUSION@#Up-regulating NOS-NO signaling may be the mechanism of Tongxinluo on cell viability and TF in AngII induced vacular endothelial cells.