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1.
Chinese Journal of Cardiology ; (12): 955-961, 2013.
Article in Chinese | WPRIM | ID: wpr-356494

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the involvement of heme oxygenase (HO-1) in PM2.5 induced toxic responses in human umbilical vein endothelial cells (HUVECs).</p><p><b>METHODS</b>The experiment groups are as follows: (1) control group; (2) PM2.5 groups: the cells were cultured with various concentrations of PM2.5 (200, 400, 800 µg/ml) for 24 h and 400 µg/ml was chosen for the main study; (3) PM2.5+Trion group: the cells were pre-treated by 10 µmol/L Trion [a scavenger of reactive oxygen species(ROS)] for 1 h before PM2.5 (400 µg/ml) treatment for 24 h; (4) PM2.5+ZnPP group: the cells were pretreated by HO-1 inhibitor ZnPP (10 µmol/L) for 1 h before treatment with PM2.5 (400 µg/ml) for 24 h. MTT assay was used to detect cell viability. Reverse transcription polymerase chain reaction (RT-PCR) and indirect immunofluorescence assay were used to determine the mRNA and protein expressions of HO-1. Fluorescence labeling probe method was used to measure intracellular ROS level and flow cytometry was used for cell apoptosis. Colorimetric assay was used to detect intracellular caspase-3 activity.</p><p><b>RESULTS</b>Compared with control, PM2.5 significantly decreased cell viability, increased intracellular ROS, cell apoptosis and caspase-3 activity (all P < 0.05), these effects were significantly attenuated in PM2.5+Tiron group while enhanced in PM2.5+ZnPP group (all P < 0.05 vs. PM2.5 group). PM2.5 upregulated HO-1 mRNA and protein expressions in HUVECs which was downregulated in both PM2.5+Tiron group and PM2.5+ZnPP group.</p><p><b>CONCLUSION</b>PM2.5 could induce oxidative injury through increasing ROS production via modulating HO-1 mRNA and protein expressions, the injury could be aggravated with inhibition of the activity of HO-1 suggesting a potential protective role of HO-1 against PM2.5 induced oxidative stress in HUVECs.</p>


Subject(s)
Humans , Cells, Cultured , Heme Oxygenase-1 , Metabolism , Human Umbilical Vein Endothelial Cells , Oxidative Stress , Particle Size , Particulate Matter , Protoporphyrins , Pharmacology
2.
Chinese Journal of Cardiology ; (12): 864-868, 2012.
Article in Chinese | WPRIM | ID: wpr-326403

ABSTRACT

<p><b>OBJECTIVE</b>To explore the mechanism of fine particulate matter (PM(2.5)) induced endothelial injury and the efficacy and mechanism of ginsenoside Rg1 on the inhibition of endothelium injuries in human endothelial cells exposure to PM(2.5).</p><p><b>METHODS</b>Human umbilical vein endothelial cells (HUVECs) were stimulated with various concentrations PM(2.5) (0.1, 0.2, 0.4, 0.8 mg/ml) and PM(2.5) at concentration 0.8 mg/ml induced significant endothelial injury and was chosen for the main study in the presence or absence of Rg1 (0.04 mg/ml). After 24 h treatment, cell growth A value was detected through MTT, intracellular reactive oxygen species (ROS) level through fluorescence labeling probe method and HO-1, Nrf2 mRNA expression was detected by RT-PCR.</p><p><b>RESULTS</b>The cell A value was significantly lower while the ROS fluorescence gray value and the average optical density ratio of HO-1 were significantly higher in PM(2.5) group than in the control group (all P < 0.05). The average optical density ratio of Nrf2 was similar between PM(2.5) group and control group (P > 0.05). The A value and the average optical density ratio of HO-1 were significantly higher while the ROS fluorescence gray value was significantly lower in co-treated PM(2.5) (0.8 mg/ml) + Rg1 (0.04 mg/ml) group than in the PM(2.5) (0.8 mg/ml) group (all P < 0.05).</p><p><b>CONCLUSION</b>PM(2.5) could induce human endothelial cells injury by increasing oxidative stress which could be attenuated by ginsenoside Rg1.</p>


Subject(s)
Humans , Cells, Cultured , Ginsenosides , Pharmacology , Heme Oxygenase-1 , Metabolism , Human Umbilical Vein Endothelial Cells , Metabolism , NF-E2-Related Factor 2 , Metabolism , Oxidative Stress , Particulate Matter , Toxicity
3.
Chinese Journal of Medical Genetics ; (6): 297-298, 2004.
Article in Chinese | WPRIM | ID: wpr-328891

ABSTRACT

<p><b>OBJECTIVE</b>To understand the allele structure and genetic polymorphism at D3S1358, D13S317, D5S818 short tandem repeats (STRs) loci in Nongqu Mongolian of China, and to construct a preliminary database.</p><p><b>METHODS</b>The allele frequencies of the three STRs loci in 291 unrelated individuals from Nongqu Mongolian were analyzed by polymerase chain reaction and polyacrylamide gel electrophoresis.</p><p><b>RESULTS</b>Six, ten, and eight alleles were observed at D3S1358, D13S317, D5S818, respectively, and all 3 loci met Hardy-Weinberg equilibrium. The statistical analysis of 3 STR loci showed the heterozygosity >or=0.7332, the polymorphic information content >or=0.6884; the combined discrimination power and the probabilities of paternity exclusion were 0.9991 and 0.9806 respectively.</p><p><b>CONCLUSION</b>All three of the loci in this study were found to have high heterozygosity and polymorphic information content, so they could provide useful markers for genetic purposes. These results could serve as valuable data to enrich the Mongolian genetic database and play an important role in Chinese population genetic application.</p>


Subject(s)
Humans , Chromosome Mapping , Mongolia , Ethnology , Polymorphism, Genetic , Tandem Repeat Sequences
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