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1.
China Pharmacy ; (12): 40-45, 2019.
Article in Chinese | WPRIM | ID: wpr-816746

ABSTRACT

OBJECTIVE: To study the effects of serglycan (SRGN) on drug resistance of ovarian cancer and its mechanism. METHODS: Gene expression profile interactive analysis tool (GEPIA) was used to extract related data set of ovarian cancer and analyze the difference of mRNA expression of SRGN between normal ovary tissue and ovarian cancer tissue. Gene expression database (GEO) was adopted to obtain the difference of the mRNA expression of SRGN in cisplatin sensitive and cisplatin resistant cell lines (A2780). STRING online database was used to screen proteins interacting with SRGN (confidence degree: 0.900, interactors: 10). Adopted biological information annotation database (DAVID) to analysis Kyoto encyclopedia of genes and genomers(KEGG)metabolism pathway to predict the potential pathways of SRGN regulating drug resistance of ovarian cancer. Medical ontology information retrieval platform COREMINE was used to mine the biological processes of significant relationship of SRGN and ovarian cancer with drug resistance. RESULTS: mRNA expression of SRGN in ovarian cancer tissue was significantly higher than normal ovarian tissue (P<0.05). mRNA expression of SRGN in cisplatin resistant ovarian cancer was significantly higher than cisplatin sensitive ovarian cancer (P<0.001). 10 proteins interacting with SRGN were screened, including albumin, transforming growth factor β1, platelet factor 4, fibrinolysin and vascular endothelial growth factor A. SRGN participated in KEGG metabolism pathway of regulating drug resistance of ovarian cancer, including HIF1α pathway, cytokine-cytokine receptor pathway, coagulation and complement cascades pathway, etc. Biological processes included gene expression, cell growth, apoptosis and cell death. CONCLUSION: SRGN mediates drug resistance of ovarian cancer, which is associated with HIF1α signaling pathway and cytokine-cytokine receptor pathway.

2.
Journal of Biomedical Engineering ; (6): 1141-1145, 2015.
Article in Chinese | WPRIM | ID: wpr-357905

ABSTRACT

Hematopoietic stem cells (HSCs) are tissue specific stem cells that replenish all mature blood lineages during the lifetime of an individual. Hematopoietic cell clusters in the aorta of vertebrate embryos play a pivotal role in the formation of the adult blood system. Recently, people have learned a lot about the embryonic HSCs on their development and homing. During their differentiation, HSCs are regulated by the transcription factors, such as Runx1 and Notch signaling pathway, etc. MicroRNAs also regulate the self-renewal and differentiation of hematopoietic stem/progenitor cells on the post-transcriptional levels. Since the onset of circulation, the formation of HSCs and their differentiation into blood cells, especially red blood cells, are regulated by the hemodynamic forces. It would be of great significance if we could treat hematologic diseases with induced HSCs in vitro on the basis of fully understanding of hemotopoietic stem cell development. This review is focused on the advances in the research of HSCs' development and regulation.


Subject(s)
Humans , Blood Cells , Cell Biology , Cell Differentiation , Embryonic Stem Cells , Cell Biology , Hematopoietic Stem Cells , Cell Biology , Signal Transduction , Transcription Factors , Physiology
3.
Journal of Biomedical Engineering ; (6): 321-325, 2015.
Article in Chinese | WPRIM | ID: wpr-266678

ABSTRACT

Hyperuricemia is a risk factor for various diseases, but knowledge on acute hyperuricemia is still not sufficient. The present study was aimed to investigate the effect of acute hyperuricemia on red blood cells from hemorheological point of view, and to provide the reference for clinical treatment. The rats were gavaged with 500 mg/kg hypoxanthine and intraperitoneally injected with 100 mg/kg oxonate to induce the model of acute hyperuricemia. The same volume of blood samples were drawn within time period of 0, 1, 2, 3 and 6 h, respectively, from the inner canthus of rats to measure the serum uric acid, hemorheological parameters and the malondialdehyde level. It was found that in each period of 1, 2 and 3 h, the rats had significantly higher levels of uric acid. The integrated deformation index and relax index were increased. The hemolysis rate was significantly reduced. The plasma malondialdehyde level was obviously decreased at the end of 2 h. The results suggested that short-term elevated uric acid could improve the hemorheological parameters and the lipid oxidative level in red blood cells.


Subject(s)
Animals , Rats , Erythrocytes , Hemorheology , Hyperuricemia , Blood , Malondialdehyde , Blood , Rats, Sprague-Dawley , Uric Acid , Blood
4.
Chinese Journal of General Surgery ; (12): 665-667, 2010.
Article in Chinese | WPRIM | ID: wpr-387826

ABSTRACT

Objective To investigate Lovastatin's effects on proliferation and adhesion of human umbilical vein endothelial cells (HUVECs). Methods Culture medium with different concentration of Lovastatin(0.001、0.01、0.1、1.0、10μmol/L) was prepared, HUVECs was cultured in 96 well-plate with the different medium. AT the point of 24,72 and 120 h, the cell's activity and quantity was assessed by MTT. HUVECs was cultured with Lovastatin in 6 well-plate for 24 hours, then collected the cells by trypsin digestion. The cells were seeded in 24 well-plate with 2×104/ml and adhering for 30 mins. Then counting the adhered cells in different wells. Results At 24 h, Lovastatin (0.01、 0.1 μmol/L ) promoted proliferation of HUVECs ( P < 0.05 ); at 72 h, Lovastatin ( 1.0μmol/L) was positive accelerating cell growth(P< 0.05 ). While Lovastatin ( 10μmol/L) inhibited the proliferation significantly ( P <0.05 ) at 120 h. As HUVECs was cultured with Lovastatin for 24 hours, Lovastatin (0.1、1μmol/L) inhanced the adhesion capability of HUVECs significantly( P< 0.05 ). Conclusion Lovastatin had biphasic effects on proliferation and adhesion of HUVECs dependent on the concentration. Lovastatin (0.1、1.0 μmol/L) could promote the proliferation and adhesion, while at higher concentration ( 10.0μmol/L) it inhibits cell proliferation and adhesion.

5.
Journal of Biomedical Engineering ; (6): 449-452, 2004.
Article in Chinese | WPRIM | ID: wpr-291091

ABSTRACT

The changes in the cellular main components of the mouse erythroleukemia cell line MEL for TFAR19 gene transfection were studied by the technology of Fourier transform infrared spectroscopy (FTIR). Using the method of gene transfection with liposome, we obtained MEL-TF19 cell line, which stably carries TFAR19, a novel apoptosis-related gene. The expression of the gene on mRNA level was confirmed by RT-PCR. Then, FTIR spectra of the cells were measured in the course of apoptosis induced by serum deprivation. Our results indicated that after being transfected with TFAR19 gene, MEL-TF19 cells exhibited relatively higher protein content, higher transcriptional activity, and relatively lower phospholipid content as compared with those exhibited by MEL cells. All the above changes reflect the apoptosis-promoting effect of TFAR19 gene, and maybe account for the cellular rheological changes after TFAR19 gene transfection, which were discovered in our previous study.


Subject(s)
Animals , Mice , Apoptosis , Genetics , Apoptosis Regulatory Proteins , Cell Line, Tumor , Genes, Tumor Suppressor , Leukemia, Erythroblastic, Acute , Genetics , Pathology , Molecular Sequence Data , Neoplasm Proteins , Genetics , Pharmacology , Spectroscopy, Fourier Transform Infrared , Transfection
6.
Chinese Journal of Medical Physics ; (6): 239-240,242,256, 2000.
Article in Chinese | WPRIM | ID: wpr-605027

ABSTRACT

Rabbit blood samples were exposed to constant magnetic field within a range of intensity from 0.05 T to 0.35 T for 10 to 50 minutes, the propersities of hemorheology were measured by ektacytometry. The following results were obtained: The blood viscosity was lowed;The RBCs deformability was not changed obviously except for 10 minutes of exposure when the RBC's deformability was strongly decreased; The orientation index was increased; The results indicate that the magnetic field increases the RBC surface charge and results in the decrease of blood viscosity.

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