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Ureteral stents play an important role in the treatment of ureteral strictures. It supports the narrow urethra and ensures the smooth flow of urine, thus alleviating the impact of ureteral stricture on kidney function. Traditional ureteral stents are prone to complications such as stones, bacterial infections, inflammation, and restenosis when indwelling in the body. This paper reviews the performance requirements of ureteral stents, introduces ureteral stents of different structures, functions, materials, and preparation as well as processing techniques, and analyzes the key problems and future research directions of ureteral stents, which provides a reference basis for the research of ideal ureteral stents.
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Aim To investigate the role of HIF-1 αin PC1 2 cell injury induced by quinolinic acid.Methods PC1 2 cells were treated with quinolinic acid at the do-ses of 2.5,5 and 1 0 mmol·L -1 ,the cell viability was determined by MTT reduction assay and LDH as-say,the intracellular levels of oxygen species was measured by assessing SOD and MDA levels,cell ap-optosis was determined by Hoechst 33258 staining,the intracellular distribution of HIF-1 αwas examined by HIF-1 αimmunostaining,and the expressions of HIF-1 α,Akt,p-Akt,Bcl-2 and Bax were determined by im-munoblotting analysis.Results Quinolinic acid in-duced cell injury in PC1 2 cells in a dose-dependent manner,and potentiated oxygen radical production and cell apoptosis.In addition,quinolinic acid enhanced HIF-1 αexpression and accumulation in nuclei.The p-Akt expression and Bax/Bcl-2 ratio was increased by quinolinc acid in PC1 2 cells.Conclusions HIF-1 αand Akt mediate qunolinc acid-induced cell apoptosis in PC1 2 cells.And cellular oxidative stress may con-tribute to the injury as well.
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Objective:To explore the effect of intratracheal transplantation human umbilical cord blood mesenchymal stem cells on pulmonary interstitial fibrosis by bleomycin in mice,compare the treatment in pulmonary fibrosis of intratracheal transplantation with tail vain injection human umbilical cord blood mesenchymal stem cells.Methods:The second generation of HUCBMSCs were cultured to the fourth generation.Sixty specific pathogen free male Kunming mice were randomly divided into 4 groups:negative control group ( Cont group) ,bleomycin group( BLM group) ,HUCBMSCs transplantation groupⅠ( MⅠgroup) and HUCBMSCs transplantation groupⅡ(MⅡ group),each group 15 mice.Pulmonary fibrosis models were induced by bleomycin via intratracheal perfusion in the latter three groups.Twenty four hours after model establishment,5-bromo-2-deoxyuridine( Brdu) marked HUCBMSCs were poured in trachea in MⅠgroup ,the same were injected into tail vein in MⅡ group.At the 7th,14th,28th day,5 mice in each group were executed re-spectively.The morphological changes of the lung tissues were observed by HE staining and Masson staining.The localization and distribution of human umbilical cord blood mesenchymal stem cells were determined by the method of immunohistochemistry.The hydroxyproline contents were measured by alkali hydrolysis assay.The protein levels of transforming growth factor β-1 ( TGF-β1 ) and smooth muscle alpha-actin(α-SMA) were detected by Western blot.Results:In the two mesenchymal stem cell transplantation groups, there were Brdu marked cells at the 7th,14th,28th days in lung tissue.The alveolitis and fibrosis in lung of the two mesenchymal stem cell transplantation groups were milder than which of the the bleomycin group(PMⅠ,MⅡgroup>Cont group(P0.05).Conclusion:The colonization of human umbilical cord blood mesenchymal stem cells can be seen in the damaged tissue via intratracheal transplantation which can alleviate pulmonary fibrosis in mice caused by bleomycin.
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Objective To investigate the expression of interleukin (IL)-34/colony stimulating factor(CSF)-1R in the process of transforming growth factor ( TGF)-β1 inducing epithelial-mesenchymal transition ( EMT) of human alveolar epithelial cells A549 cells.Methods A549 cells were cultured in vitro.CCK 8 was used to test the influence of the proliferative rate of A549 cells which were stimulated by TGF-β1 at different concentrations and time points .A549 cells were stimulated by 5μg/L TGF-β1 at 0 hour, the 12th hour, the 24th hour, and the 48th hour.Western blotting was adopted to detect changes of the following proteins: α-smooth muscle actin (α-SMA ) , E-cadherin ( E-Cad ) , matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1(TIMP-1). Real-time PCR was adopted to detect changes of the following genes: IL-34 mRNA, CSF-1R mRNA, MMP-2 mRNA and MMP-9 mRNA.Results TGF-β1 had no significant influence in the proliferation of A 549 cells compared with the control group(P>0.05).TGF-β1(5μg/L)stimulated A549 cells at different time point (0 hour, 12, 24, 48 hours), compared with the control group .The epithelial phenotype E-Cad protein was gradually down-regulated ( P <0.01 ) , while the mesenchymal phenotype α-SMA protein was gradually up-regulated ( P <0.01 ) and the protein of MMP-2 increased gradually (P<0.01).The protein of MMP-9 increased firstly and then was reduced (P<0.01),the peak was at the 24th hour.The protein of TIMP-1 was firstly transiently increased and then reduced (P<0.01), the minimum was at the 48th hour.Compared with the control group , the gene of IL-34 mRNA increased gradually (P<0.01), and the genes of CSF-1R mRNA, MMP-2 mRNA and MMP-9 mRNA increased firstly and then decreased ( P <0.01), which were peaked respectively at the 24th hour, the 24th hour, the 12th hour, respectively.Conclusion In the process of TGF-β1 inducing A549 cells transition,there is accompanied with the expression of IL-34/CSF-1R.
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BACKGROUND: As the end product of lipid peroxidation, malondialdehyde (MDA) content can be used for assessment lipid peroxidation injury.Glutathione peroxidase (GSH-Px) acts as a free radical scavenger. Currently the effect of static magnetic field on the organism, whether positive or negative, has not been elucidated.OBJECTIVE: To study the effect of static magnetic field on anti-oxidation capacity of mouse hepatic tissues and its intensity dependence for producing such effects.DESIGN: A controlled comparative experiment.SETTING: Laboratories of Medical Physics and Biochemistry of Jiangsu University.MATERIALS: The experiment was conducted in the Laboratories of Medical Physics and Biochemistry of Jiangsu University from January to December 2003. Totally 30 mice of either sex weighing 18-20 g were selected and subjected to magnetic filed exposure using a self-designed ferrite magnet apparatus.METHODS: The mice were equally randomized into normal control group and 4 exposure groups exposed to magnetic field of (24.6±4.2) mT,(42.0±2.1) mT, (63.5±3.0) mT, and (85.1±2.9) mT, respectively. The mice in the 4 exposure groups were exposed to static magnetic field of the specified intensity for 2 hours twice a day, while those in the normal control group were subjected to the sham exposure apparatus without magnetic field at scheduled time points every day. After 15 days of exposure, the mice were sacrificed and the GSH-Px activity and the MDA content in the hepatic tissue were assayed.MAIN OUTCOME MEASURES: GSH-Px activity and MDA content in hepatic tissue of the mice.RESULTS: Thirty mice entered the final analysis without losses. MDA content in (24.6±4.2) mT and (42.0±2.1) mT groups were obviously lower than that in the normal control group [(12.70±0.53), (12.96±0.72), and (17.62±0.91) μmol/g, respectively, F=10.4, 9.89, P ＜ 0.01]. The GSH-Px activity in the hepatic tissue in (24.6±4.2) mT and (42.0±2.1) mT groups were obviously higher than that in the normal control group [(143.36±8.34),(150.69±12.00), (87.51±11.34) μkat/g, respectively, F=10.0, 11.3, P ＜ 0.01].CONCLUSION: Static magnetic field of appropriate intensity can lower MDA content and enhance the GSH-Px activity in the hepatic tissue of mice, and may also improve the activity of antioxidase and reduce the production of lipid peroxidation to diminish the consequent injuries and delay the aging process.
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Objective To study the effect of static magnetic field (SMF) on levels of lipid peroxidation in liver kidney and brain tissues in mice. MethodsThirty mice were randomly assigned to groups A,B,C and D, and exposed to static magnetic fields with four different intensities of(24.6?4.2)mT, (42.0?2.1)mT, (63.5?3.0)mT, (85.1?2.9)mT, respectively, for an average of 4 hours daily for 15 days. Then the mice were sacrificed and the amount of MDA in liver, kidney and brain tissues in mice were measured. ResultsThe amount of MDA were significantly decreased in the liver and kidney in rat exposed to (24.6?4.2)mT, (42.0?2.1)mT MSF as compared with that in the control group( P
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Objective To study the effect of static magnetic fields on the micronucleus in polychromatic erythrocytes(PCE) in the bone marrow and and the lipid peroxidation in the brain tissue in mice.Methods Fourty Kunming mice were randomly divided in to the negative control group,positive control group(cyclophosphamide:145 mg/kg) and the static magnetic fields(20,40,50,60,80 and 100 mT) exposure group,exposed twice a day,for two hours each time.After 15 days,the micronuclei rate of the bone marrow,blood cells and the activity of superoxide dismutase(SOD),the protein malonaldehyde(MDA) were determined.Results Compared with the control,the micronuclei rate in 50,60,80 and 100 mT exposure group increased significantly,the amount of leukocyte significantly decreased,the activity of SOD in the brain tissue in 60,80 and 100 mT exposure group decreased and the content of MDA increased significantly.Conclusion The present experiment demonstrats that static magnetic fields exposure at doses of 50,60,80 and 100 mT may induce the micronuclei rate increase,the amount of leukocyte decrease,the activity of SOD in the brain tissue decrease and the content of MDA increase.
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Objective To study the effects of static magnetic field (SMF) on development of rat embryonic spinal cord neurons. Methods Primary cultured embryonic spinal cord neurons of Wistar rat were exposed to 1.0, 10.0, 50.0, 100.0 and 200.0 mT static magnetic field. The morphological structure, cell's differentiation and proliferation of the embryonic spinal cord neurons were observed and the contents of MDA, superoxide dismutase (SOD) and protein contents in the neurons were determined. Results Static magnetic field at density of 50-200.0 mT could inhibit the differentiation and proliferation of the cells and the phenomena such as cell aggregation, detouchment of some cells, decrease of clone-formation rate and the size of the cells were observed. The contents of MDA in the cells were increased, while the activities of SOD and the level of protein were decreased. Conclusion Static magnetic field might damage the development of embryonic spinal cord neurons by enhancing the lipid peroxidation.
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Objective To approach the effect of acrylonitrile (ACN) on the proliferation and differentiation of the lung fibroblasts of mice. Methods The purification and primary culture of the lung fibroblasts(LFb)of new born mice were conducted. The cells were treated with ACN added in the medium at the varying doses of 0.01, 0.5, 1.0, 10.0, 50.0, 100.0 and 200.0 ?g/ml. The cytomorphological methods were used, the protein, malonaldehyde (MDA) and the activity of superoxide dismutase (SOD) were determined. Results No inhibitted effect on the lung fibroblasts was observed at the doses of 0.01-10.0 ?g/ml. At the doses of 50.0-200.0 ?g/ml, acrylonitrile could inhibit the differentiation and proliferation of the cells, the volume of cells became small,the rate of cell clusters decreased, at the doses of 10.0-200.0 ?g/ml, the content of protein and the activity of SOD decreased, MDA content increased. Conclusion Acrylonitrile can inhibit the proliferation and differentiation of the lung fibroblasts in mice, protein synthesis inhibition and lipid peroxidation are considered as the related factors.