ABSTRACT
Objective To investigate the relationship between aldehyde dehydrogenase 2 (ALDH2) gene polymorphism and premature coronary heart disease (CHD) in Chinese Han population.Methods A total of 505 patients were enrolled in the present study.Of them,375 were definitely diagnosed as CHD and another 130 were excluded from CHD by coronary angiography.Coronary heart disease patients were divided into premature coronary heart disease (male ＜55 years,female ＜65 years) group (n=150) and late onset coronary heart disease (male ≥ 55 years,female ≥ 65 years) group (n=225);According to whether after drinking flushing,the enrolled 505 patients were divided into alcohol flushing syndrome(AFS) group (n=135) and no AFS group (n=370);According to whether used to drinking,they were divided into accustomed to drinking group (n=189) and no drinking custom group (n=316).The ALDH2 gene polymorphism was analyzed by sanger sequencing.Results There was no significant difference in the distribution ofALDH2 genotype between the patients with premature CHD and late-onset CHD,also between CHD and non-CHD (P＞0.05).The logistic regression analysis showed that ALDH2 gene was not a predisposing factor of PCHD and CHD after adjusting for gender,age,smoking,drinking,body mass index (BMI),hypertension,diabetes,hyperlipidemia and family history of CHD (P=0.729,OR=1.098,95％CI 0.648-1.859;P=0.581,OR=1.156,95％CI 0.692-1.930).The incidence of ALDH2 mutant (GA+AA) was significantly higher in AFS group than in no AFS group (67.4％ vs.10.5％,P＜0.01).The gene mutation frequency was markedly higher in no drinking custom group than in accustomed to drinking group (29.7％ vs.19.1％,P＜0.01).Conclusions No obvious correlation exists between ALDH2 gene polymorphism and the incidence of premature CHD or the onset of CHD in Chinese Han population.There is a certain relationship between ALDH2 mutant gene and AFS.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the mechanisms underlying the incorporation of microparticles(MP) derived from human bone marrow mesenchymal stem cells (MSCs) into human umbilical cord endothelial cells (HUVECs).</p><p><b>METHODS</b>MPs were isolated from the supernatants of MSCs which had exposed to a hypoxia/serum-deprivation condition. Electron microscope was used to identify the MPs. The surface molecule profile was evaluated with the bead-based flow cytometry technique. The expression level of the phosphatidylserine receptor (PSR) was detected by immunofluorescence cytochemistry. MPs were co-cultured with HUVECs in the presence or absence PSR-antibody, and the internalization of MPs was observed with laser scanning microscopy.</p><p><b>RESULTS</b>The MPs derived from MSCs expressed highly PS, while PSR expressed on the surface of HUVECs. The confocal result revealed that MPs could quickly be uptaken by the endothelial cells, and mainly distributed in the cytoplasm surrounding of the nuclei. The internalization of MPs reduced significantly after PSR specific blockage.</p><p><b>CONCLUSION</b>The reaction between PS on the MP and the PSR of HUVECs plays an important role in the internalization of MSC-MPs.</p>
Subject(s)
Humans , Cells, Cultured , Coculture Techniques , Endothelial Cells , Flow Cytometry , Mesenchymal Stem Cells , Umbilical CordABSTRACT
<p><b>OBJECTIVE</b>To investigate the protection of silymarin against the human mesenchymal stem cell (MSC) apoptosis induced by serum deprivation and its underlying mechanism.</p><p><b>METHODS</b>Human umbilical cord MSCs were cultured in the absence of serum, and the silymain of different concentration (1-10 µg/ml) was added into the medium. MTT test was performed to observe the cell proliferation status. After being cultured for 72 hours, the cells were collected, and flow cytometry with Annexin-V-PI double-staining was used to detect the apoptotic cells from the control and silymarin-treated groups. Furthermore, the intracellular contents of BAX and BCL-2 were detected by Western blot for exploring the potential mechanism.</p><p><b>RESULTS</b>The silymarin promoted the proliferation of human UC-MSCs in a dose-dependent manner, reaching its maximal at a dose of 5 µg/ml. Moreover, silymarin could inhibit the serum deprivation-induced apoptosis of MSCs and, the inhibitory rate reached up to 30% when it was added at a concentration of 5 µg/ml. The content of intracellular BAX was obviously elevated after serum-deprivation treatment, and this increase could be blunted by the addition of silymarin. Meanwhile, the content of BCL-2 was not obviously changed.</p><p><b>CONCLUSION</b>The silymarin can stimulate MSC growth and inhibit the apoptosis of MSCs probably by the mitochondria pathway.</p>