Texts of Kolima dialect of Yukaghir

<p>Clinical chemistry data of monkeys fed on diets containing GM rice or non-GM rice.</p

Additional file 3: of A preliminary study showing no association between methylation levels of C3 gene promoter and the risk of CAD

Table S3. Subgroup analysis of methylation levels of CpG sites in C3 promoter between CAD and controls by smoking status. Table S4. Subgroup analysis of methylation levels of CpG sites in C3 promoter between CAD and controls by EH status. Table S5. Subgroup analysis of methylation levels of CpG sites in C3 promoter between CAD and controls by DM status. (ZIP 34.7 kb

Additional file 1: of A preliminary study showing no association between methylation levels of C3 gene promoter and the risk of CAD

Table S1. Methylated CpG sites measured in this study. (DOCX 12.8 kb

Additional file 3: of Serum PCSK9 levels, but not PCSK9 polymorphisms, are associated with CAD risk and lipid profiles in southern Chinese Han population

Figure S2. Associations between PCSK9 E670G polymorphism and PCSK9 levels (A. in whole population; B. in case and controls subgroups; C. in male and female subgroups; D. in elderly and non-elderly subgroups; E. in EH and non-EH subgroups; F. in DM and non-DM subgroups). (ZIP 67 kb

Additional file 2: of Serum PCSK9 levels, but not PCSK9 polymorphisms, are associated with CAD risk and lipid profiles in southern Chinese Han population

Figure S1. The genemapper analyses of genotypes of PCSK9 polymorphisms (A. E670G AA genotype; B. E670G AG genotype; C. E670G GG genotype; D. R46L GG genotype). (ZIP 7 kb

Additional file 1: of Serum PCSK9 levels, but not PCSK9 polymorphisms, are associated with CAD risk and lipid profiles in southern Chinese Han population

Table S1. The sequence of PCR primers. Table S2. The sequence of probes used in the study. (DOCX 16 kb

Effect of triptolide and SFN on nuclear levels of Nrf2 in livers of BALB/C mice.

<p>Nuclear protein lysates were made from livers of mice from different experimental groups and subjected to Western blot analysis using the indicated antibodies. The histone H3 was used as an internal control. A representative blot from three independent experiments is shown. The density of the immunoreactive bands was analyzed, and the data are represented as the means ± SD; n = 6; *<i>P<0.05</i> versus Con group.</p

siRNA-Nrf2 enhances triptolide-induced oxidative stress in HepG2 cells.

<p>HepG2 cells transfected with siRNA-control or siRNA-Nrf2 were treated with triptolide at various concentrations for 6 h. (A) Levels of intracellular GSH were measured. (B) The intracellular ROS levels were measured using the fluorescent probe DCFH-DA.The data are represented as the mean ± SD from three independent experiments. *<i>P</i><0.05, **<i>P</i><0.01 versus vehicle control; ^#<i>P</i><0.05, ^##<i>P</i><0.01 versus si-control cells treated with the same concentration of triptolide. Con: control (0.1% DMSO).</p

Activation of Nrf2 Protects against Triptolide-Induced Hepatotoxicity

<div><p>Triptolide, the major active component of <i>Tripterygium wilfordii</i> Hook f. (TWHF), has a wide range of pharmacological activities. However, the toxicities of triptolide, particularly the hepatotoxicity, limit its clinical application. The hepatotoxicity of triptolide has not been well characterized yet. The aim of this study was to investigate the role of NF-E2-related factor 2 (Nrf2) in triptolide-induced toxicity and whether activation of Nrf2 could protect against triptolide-induced hepatotoxicity. The results showed that triptolide caused oxidative stress and cell damage in HepG2 cells, and these toxic effects could be aggravated by Nrf2 knockdown or be counteracted by overexpression of Nrf2. Treatment with a typical Nrf2 agonist, sulforaphane (SFN), attenuated triptolide-induced liver dysfunction, structural damage, glutathione depletion and decrease in antioxidant enzymes in BALB/C mice. Moreover, the hepatoprotective effect of SFN on triptolide-induced liver injury was associated with the activation of Nrf2 and its downstream targets. Collectively, these results indicate that Nrf2 activation protects against triptolide-induced hepatotoxicity.</p></div

Effect of triptolide and SFN on activities of antioxidant enzymes in liver of BALB/C mice.

<p>Mice were given vehicle control, SFN (25 mg/kg), TP (1.0 mg/kg), SFN (25 mg/kg)+TP (1.0 mg/kg) by intraperitoneal injection. Mice were sacrificed under anesthesia 24 h after triptolide treatment. Values are expressed as mean ± SD. n = 6.</p>a<p><i>P<0.05</i> compared to the control group.</p>b<p><i>P<0.01</i> compared to the control group.</p>c<p><i>P<0.05</i> compared to the triptolide-treated group.</p>d<p><i>P<0.01</i> compared to the triptolide-treated group.</p