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Table of Content

    25 January 2009, Volume 29 Issue 1
    研究论文
    MR1 siRNA suppresses the proliferation of human hepatoma BEL-7402 cells
    Jin-hua WANG; Chun-jing BIAN; Chun-hua ZHAO
    2009, 29(1):  1-5. 
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    Objective To identify the function and mechanism of MR1 in proliferation of BEL-7402 cells. Methods siRNA targeting MR1 and negative control siRNA were chemically synthesized, and transfected into BEL-7402 cells using Lipofectamine 2000. The silencing effect of MR1 siRNA was determined by semi RT-PCR. SRB assay, colony formation assay and growth curve assay were used to investigate whether MR1 siRNA regulated cellular proliferation. Cell cycles were assessed by flow cytometry. G2 arrest reagent nocodazole was used to show the possible effect of MR1 siRNA on G1 arrest. The expression of Cyclin D1 was determined by Western blotting. Results ①MR1 mRNA decreased significantly in BEL-7402 cells 24h after MR1 siRNA transfection. ②MR1 siRNA induced the down-regulation of cell growth. The expression level of Cyclin D1 in MR1 siRNA tranfected BEL-7402 cells decreased significantly by contrast to negative control siRNA transfected cells. ③Flow cytometry results showed that MR1 siRNA markedly decreased G2 phase population with nocodazole treatment, and distinctly increased G1 phase population. Conclusion The gene MR1 is involved in the proliferation of BEL-7402 cells. MR1 siRNA causes inhibition of the proliferation of BEL-7402 cells. One of the mechanisms of MR1 siRNA on the proliferation of BEL-7402 cells is the induction of G1 arrest.
    Relationship between mutation G4295A of MYBPC3 gene and clinical phenotype of hypertrophic cardiomyopathy in Chinese population
    Hu WANG; Yu-bao ZOU; Ji-zheng WANG; Lei SONG; Kai SUN; Xiao-dong SONG; Ru-tai HUI
    2009, 29(1):  6-9. 
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    Objective To study the disease-causing gene mutations in Chinese hypertrophic cardiomyopathy (HCM) and to reveal the relationship between the genotype and the phenotype. Methods One hundred unrelated patients with HCM and 120 controls were chosen for the study. The full encoding exons and flanking sequences of the cardiac myosin binding protein C gene (MYBPC3) were amplified with PCR and the products were sequenced. The relation between genotype and phenotype was analyzed. Results Mutation G4295A was identified in exon 6 of MYBPC3 gene in two families, which resulted in the glutamic acid (E) converted to lysine (K). Echocardiography showed no obstruction of left ventricular outflow tract in the two HCM probands. This mutation (E258K) resulted in mild HCM phenotypes and showed low penetrance. The 120 controls were normal in the genetic test. Conclusions The G4295A mutation of MYBPC3 gene is the causal mutation of familial HCM with mild phenotype.
    Sca1+ mesenchymal stem cells induce hemopoietic stem cells to differentiate into dendritic cells
    Yuan CHEN; Xing-xia LIU; Chun-hua ZHAO
    2009, 29(1):  10-13. 
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    Objective Study the effect of Sca1+ cells on the HSCs`(hemopoietic stem cells) differentiation to dendritic cells (DCs), and identify the morphology, function and surface markers of the cells. Methods CD117+ HSCs were isolated and purified from the bone marrow of healthy Balb/c mice by magnetic affinity cell sorting. After cell expansion by treatment with the support of Sca1+ cells, the HSCs were induced for directional differentiation into DC-like cells.Studied the surface markers by FACS and function via LSCM and animal experiments. Results After 10 days of culture , we demonstrated that Sca1+ cells induced HSCs to differentiate into a distinct regulatory DC subset with high expression of CD11b but low expression of Ia. They had phagocytotic activity,and can suppressed the GVHD(graft versus host disease) reaction. Conclusion HSCs can differented to dendritic cells with the support of Sca1+ cells.
    Characterization of ligand-binding properties of PDZ domain of Veli3 by screening random peptide library
    Rui TIAN; Su-can MA; Tao YANG; You-he GAO
    2009, 29(1):  14-18. 
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    Objective To investigate the ligand-binging characteristics of Veli3 PDZ. Methods Random peptide library was screened using yeast two-hybrid method with Veli3 PDZ as bait. In combination with bioinformatics method all the potential ligands in human proteome have been predicted by searching human databases with the consensus-binding sequences. Fourteen native human proteins predicted as ligands were chosen by their cellular locations and biological functions for validating protein interaction in yeast two-hybrid system. Results The C-terminal consensus sequences for the Veil3 PDZ binding is [E/X][S/T]X[V/I/L]-COOH (X denotes any amino acid), which indicates that Veli3 PDZ belongs to classⅠ. Six of fourteen native human proteins predicted as ligands were confirmed positive in the yeast two-hybrid system. There are a lot of interactions between PSD-95, another PDZ protein, and the ligands of Veli3 PDZ reported previously and discovered in this study. Conclusion The six novel potential ligands of Veli3 found in this study provide significant clues for discovering biological functions of Veil3 proteins. Moreover, Veli3 PDZ and PSD-95 PDZ may compete with each other to bind the same ligands.
    Hydrogen sulfide inhibits expression of intercellular adhesion molecule-1 in the pathogenesis of atherosclerosis in apoE knockout mice
    Yan-fei WANG; Chao-shu TANG; Jun-bao DU
    2009, 29(1):  19-23. 
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    Objective To explore the effect of hydrogen sulfide (H2S) on intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of atherosclerosis in apoE knockout (apoE-/-) mice. Methods 6 week-old C57BL/6J and apoE-/- mice were divided into control C57BL/6J group, apoE-/- group, apoE-/- + sodium hydrosulfide (NaHS, a donor of H2S) group and apoE-/- + DL-propargylglycine (PPG, an inhibitor of H2S synthase). There were 8 mice in each group. They were fed chow diet for 10 weeks. Serum H2S was measured by sulfide electrode-based method, serum ICAM-1 was determined by ELISA and aortic ICAM-1 mRNA was detected by real time polymerase chain reaction. The changes of atherosclerosis plaque size were observed by oil red O staining. Results Compared with control mice, serum H2S level was significantly decreased in apoE-/- mice (P 0.01), while serum ICAM-1 and aortic ICAM-1 mRNA were markedly increased (P 0.01). The atherosclerosis plaque was obvious in apoE-/- mice. Compared with apoE-/- mice, serum H2S level was significantly increased (P 0.05), while serum ICAM-1 and aortic ICAM-1 mRNA were significantly decreased (P 0.01 and P 0.05, respectively), and the area of atherosclerosis plaque was significantly diminished (P 0.05) in apoE-/-+NaHS mice. In apoE-/-+PPG mice, serum H2S level was significantly decreased (P 0.05), while serum ICAM-1 and aortic ICAM-1 mRNA were significantly increased (P 0.05 and P 0.01, respectively), and the size of atherosclerosis plaque was significantly enlarged (P 0.01). Conclusion H2S suppressed the expression and secretion of ICAM-1 during the formation of atherosclerotic plaque.
    Establishment and characterization of healthy donor's γδT cell clones
    Xiao-juan HE; Ning KANG; Hui CHEN; Lian-xian CUI; Wei HE
    2009, 29(1):  24-28. 
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    Objective Establishment and characterization of healthy donor's γδT cell clones. Methods γδT cells were cloned by limiting dilution after positive sorting, with 60Co irradiated allogeneic PBMC as feeder cells. Flow cytometry analysis and molecular biology technique were then used to identify γδT cell clones, and MTT assay was used to verify their proliferation after incubated with epitope peptides recognized by γδT cells. Results A γδT cell clone had been established. The subtype of this clone was V γ9 V δ2 and the expression of CD4 and CD8 molecule were negative. Further studies indicated that epitope peptide EP6 could not only specifically bind γδT cell clone but also trigger the proliferation of γδT cell clone. Conclusion A healthy donor's γδT cell clone was successfully established, which laid a solid foundation for further study on γδT cells.
    Relationship between VEGF decreases cerebral ischemia/reperfusion injury and the expression of caspase-3 in rabbits
    Ji-ping YANG; Xin-feng LIU; Huai-jun LIU; Ren-liang ZHANG; Qin YIN; Yun LI
    2009, 29(1):  29-32. 
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    Objective To study the relationship between VEGF decreases focal cerebral ischemia/reperfusion injury in rabbits and the expression of cysteinyl aspirate-specific proteinase-3 (caspase-3) protein. Methods Focal cerebral ischemia/reperfusion model in rabbit was induced. The VEGF was administered at 0, 1 and 3 h after reperfusion respectively. Infarct and edema volumes, neurological deficit score, apoptotic cells, and expression of caspase-3 were assessed at 3 d after reperfusion. Results VEGF reduced infarct volumes compared with controls by 23.3% and 17.9% when administered VEGF at 0 and 1 h after reperfusion. Edema volumes, apoptotic cells and expression of caspase-3 in the perifocal regions were significantly lower than that in control group when administered VEGF within 1h after reperfusion (P<0.01). There was no difference when administered VEGF at 3h after reperfusion. Infarct volumes were correlated significantly with expression of caspase-3 in the perifocal regions (P<0.05). Conclusions The effect of VEGF on the expression of caspase-3 is related with the neuroprotective time window. The VEGF can reduce the incidence of neuronal apoptosis during the cerebral ischemia/reperfusion injury by reducing the expression of caspase-3 protein.
    Differentiation of mouse embryonic stem cells into cardiomyogenic cells cocultured with cardiomyocytes
    Wei-dong LI; Xiao-gang ZHANG; Jing CHANG; Fang-pin JIANG
    2009, 29(1):  33-37. 
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    Objective To explore the effect of embryonic stem cells(ESCs) differentiating into cardiomyocytes(CM ) by cardiomyocytes. Methods The blastocytes of 3.5d from Kunming species mouse,cultured on mouse embryonic fibroblaste cell feeder layers for 4~5d, and the mouse ESCs were isolated and subsequently cultured in vitro. Day 2~3 embryoid bodies(EBs) were derived from ESCs of passage 3 to 5 and then cocultured with neonatal cardiomyocyte(CM) to induce into cardiomyocytes and the expression of cardiac specific cardiac troponin-T(TnT) and а-Actin were detected by immunofluoresence. Result The rhythmic beating embryoid bodies were observed on day 3and reached 93% of rhythmic beating embryoid bodies on 12 day in group 2.All the beating cardiomyocytes derived from ESCs expressed cardiac-specific proteins for TnT and а-Actin, and the group induced by direct cell to cell contact acquired the highest differentiating ratio of 56.5%,and was the highest differentiating ratio compared with other groups (p<0.05).Conclusion Both cardiomyocyte coculturing system and cardiomyocyte-lysate system can induce mouse ESCs to differentiate into cardiomyocyte-like cells and the induced effect of direct cell-to-cell interaction with neonatal cardiomyocytes was higher than cardiomyocyte-lysate.
    Differential proteomic analysis of the pancreas from diabete rat
    Wei PAN; Song WU; Xing LI; Guo-zhen YANG; Fang HAN; Yi-bing YIN
    2009, 29(1):  38-41. 
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    Objective Through the proteomic approaches, this work was aimed to find useful information for the diabetogenic mechanism by the protein profiling of the pancrea of diabete rat. Methods The rat model of type 1 diabetes was acquired by STZ administration to Wistar rat, the protein profiling of pancrea was conducted by two-dimensional electrophoresis. Then comparative imaging analysis was conducted between diabetes model and control. In-gel digestion and MALDI-TOF-MS analysis were done to get peptide mass fingerprint(PMF). Lastly Mascot was used for the identification of proteins. Results 11 diferentially-expressed protein spots were excised for MS identification, and 4 proteins of them were identified as significant results. Conclusion The differential analysis of pancreas proteins between the diabete rat and control are helpful for the insight into the pathogenesis of Diabetes.
    Sodium ferulate inhibits neurons injury mediated by Aβ25-35-induced macrophage activation of mice
    Su-yan YAO; Ying JING; De-yu ZHENG
    2009, 29(1):  42-46. 
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    Objective To examine the effect and mechanism of sodium ferulate inhibiting p38MAPK in macrophage on neurotoxicity which was mediated by fribrilar -amyloid-induced. Methods The isolated peritoneal macropohages from mices were cultured . p38MAPK protein in nuclear extracts was analyzed by Western blot and production of tumor necrosis factor-α(TNF-α) was detected by ELISA. For neuron-macrophage co-cultures, Microtubute-associated protein-2(MAP-2) expression were detected by immunocytochemical technique. The level of LDH in the medium were measured. Results The production of TNF-α and p38MAPK protein in nuclear extracts increased significantly by incubation of Aβ25-35. LDH efflux in neuron-macrophage co-culture medium increased and MAP-2 expression decreased significantly(P<0.01). As to the sodium ferulate groups, however, the damages were dose-dependently eliminated (P<0.05). Conclusion Sodium ferulate could inhibit p38MAPK mediated by Aβ25-35 and decrease the production of TNF-α. Sodium ferulate could play a role in protecting the neurons against the impairments induced by Aβ25-35.
    Transdifferentiation of Rat Muscle Derived Stem Cells into Insulin-Secreting Cells in Vitro
    Chang LIU; Fu-qiang LIU; Xi-fan MEI; Biao YANG
    2009, 29(1):  47-51. 
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    Objective To explore the possibility of diferentiating functional insulin-secreting cells from muscle derived stem cells.Methods SD rat muscle derived stem cells (MDSCs)were isolated and cultured then induced for 7~12 days with combination inductor.Morphological changes of the induced cells were observed under an inveted microscope.DTZ staining ,immunocytochemical staining were conducted to examine the production of insulin. Glucose challenge and radio immunoassay were perfomed to evaluate the function of the aggregates,and RT-PCR was conducted to detect the expression of endocrine gene.Results Typical insulin-producing cells were observed at the end of the protocol(12 days). Ditizone staining and immunohistochemistry for insulin were both positive. Insulin was secreted by these cells in response to different concentrations of glucose stimulation in a regulated manner (P<0.05). RT-PCR showed the insulin,glucagon and SS gene expression on the 7th day after the inducement of combination inductor. Conclusion Insulin-secreting cells can be transdiferentiated from muscle derived stem cells,which may be a new procedure for clinical treatment of diabetes.
    Effect and its underlying mechanism of antioxidant quercetin in the mice in vivo and NIH-3T3 cells in vitro
    Cui-cui GONG; Nai-gang ZHENG; Jing-lan WU; Pei-xia HE; Yi-ling WANG
    2009, 29(1):  52-58. 
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    Objective To compare the difference in quercetin against oxidative stress response between in mouse plasma and in H2O2-pre-/post-treated NIH-3T3 cells, and to explore the underlying mechanism for the quercetin antioxidant. Methods The cultured NIH-3T3 cells were randomly divided into 4 groups: quercetin (Q) pre-protective group (Qb) firstly treated with quercetin for 24h followed by incubation with H2O2 for 30 min; post- protective group (Qa) firstly treated with H2O2 for 30 min followed by incubation with quercetin for 24h; H2O2 group (H2O2) after exposure with H2O2 for 30 min, incubated with DMEM medium and the control group (C) only cultured with DMEM medium. The survival rate and apoptotic rate were detected respectively with MTT and TUNEL in NIH-3T3 cell suspension samples. The expression of cyclin D1, PTEN, NF-kB, HSP-70, Bcl-2, Bax and caspase-3 was examined with immunocytochemistry and immunoblotting. Besides, 20 Wistar rats were divided into control group and experimental group, the latter was given with quercetin in the doze of 0.13mmol/kg. The levels of T-AOC,SOD,GSH-Px,GSH,MDA, NOS and NO2-/NO3- were detected both in the cleaved NIH-3T3 cells in vitro and in the plasma in vivo from both experimental and control animals prior to and post-1 h, 2h and after 24 h. Results When the Qb group was compared with H2O2 or Qa group, the survival rate was higher and the apoptotic rate was lower. When the H2O2 group was compared with C group,the expression of cyclin D1、PTEN or Bcl-2 was down-regulated;while that of Bax、HSP-70、NF-kB or caspase-3 was up-regulated; the level of T-AOC,SOD,GSH-Px or GSH was decreased; that of NOS、NO2-/NO3- or MDA enhanced in the cleft NIH-3T3 cells. When the Qb group was compared with Qa or H2O2 group, the reversed H2O2 effects, especially elevated the decreased A-TOC and GSH-Px and depressed the enhanced MDA effects by H2O2, were more marked. When the plasma level of the anti-oxidative enzyme system prior to- compared with post-1h and 2h-treatment with Q, the level of T-AOC, SOD, GSH-Px and GSH, especially the former two, were higher; MDA, lower; NOS or NO2-/NO3- promoted. However, the above parameters basically became normal 24h after treatment with Q. Conclusions Quercetin could down-regulate the promoted expression of HSP70, NOS, NO2-/NO3- and NF-kB etc. in H2O2-treatment NIH-3T3 cells. Qb could reverse the H2O2 damage effects more markedly, including up-regulation of PTEN expression, inhibiting PI3k/Akt signal transduction, inactivating NF-kB expression, and depressing Bcl2/Bax ratio and apoptosis through modulating cyclin D1 expression level. Moreover, the quercetin could exert anti-oxidant protective effect through modulating the anti-oxidative enzyme system both in vivo and in vitro. However, based on the cell heterogeneity in none- or pre/post-H2O2-treatment state, a difference in quercetin antioxidant response exhibited.
    Thalidomide inhibits TGF-β1-induced transdifferentiation of human fetal lung fibroblast cell line to myofibroblast
    Zhi WANG; Li-dan ZHAO; Xuan ZHANG; Fu-lin TANG; Meng-xue YU
    2009, 29(1):  59-63. 
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    Objective To investigate the effects of Thalidomide(THD)on transdifferentiation of human fetal lung fibroblast (HFL-F) to myofibroblast (MF) induced by Transforming Growth Factor-β1 (TGF-β1) and on differentiated MF. Methods HFL-F to MF differentiation was induced with 5μg/L TGF-β1. The effect of 50μg/L THD on HFL-F to MF transdifferentiation was evaluated by measuring hydroxyproline (Hyp) content with alkaline hydrolysis method, α-smooth muscle actin (α-SMA) protein with Western Blot, α-SMA and collagen Ⅲ (COL Ⅲ) mRNA with semiquantitative RT-PCR. Results THD could inhibit TGF-β1 induced up-regulation of Hyp and COL Ⅲ mRNA expressions (all p<0.05), α-SMA protein synthesis may reduced, but had no effect on α-SMA mRNA expression (p>0.05). For HFL-F treated with 5μg/L TGF-β1 for 96h, THD could inhibit COL Ⅲ mRNA expression (p<0.05). Conclusions TGF-β1 could induce HFL-F to MF transdifferentiation; THD could affect this process by inhibiting Hyp production, α-SMA protein synthesis and COL Ⅲ mRNA expression. THD could additionally inhibit COL Ⅲ mRNA expression in transdifferentiated MF.
    The inhibitory effect of Metformin on TNF-α Expression in hepatic tissue of OLETF Rats
    Ai-mei DONG; Xiao-hui GUO; Wei WANG
    2009, 29(1):  64-68. 
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    Objective To investigate the TNF-α expression in hepatic tissue of Otsuka Long-Evans Tokushima Fatty (OLETF) rats (an insulin resistance model) with abnormalities of glucose-lipid metabolism and effect of metformin on TNF-α expression. Methods OLETF rats were assigned to two groups randomly (OLETF and OLETF/M).The OLETF/M group was treated with metformin (100 mg/(kg·d)), the OLETF group and age-matched LETO (nondiabetic Long-Evans Tokushima Otsuka rats) group was fed with placebo. After 22 weeks of treatment, we analyzed rats hepatic triglyceride levels and measured expression of TNF-αby western-blot (protein) and quantitative RT-PCR(mRNA). Results After 22 weeks of treatment, the levels of fasting glucose, insulin, triglyceride, free fatty acids (FFA) and hepatic triglyceride were increased significantly in OLETF group compared with LETO group. Western-blot method showed upregulated expression of TNF-α protein in OLETF group (1.57-fold vs LETO group, P <0.05). On the mRNA level, expression of TNF-α were also elevated significantly in OLETF group (1.67-fold vs LETO group, P <0.05). Metformin reduced levels of fasting glucose, insulin, FFA and hepatic triglyceride significantly in OLETF/M group. After treatment of metformin, the expressions of TNF-α protein and mRNA in hepatic tissue downregulated (protein: 59%, P<0.05 and mRNA: 45%, P<0.05)in OLETF/M group. Conclusion The therapeutic effects of metformin on insulin resistance and fatty liver disease were associated with the significant suppression of TNF-α expression in hepatic tissue.
    The Feasibility of Bone Marrow Mesenchymal Stem Cells Transplanted Into Coronary Artery
    Geng-xu HE; Tong YAO; Hao ZHANG; Xiao-ling ZHANG; Sheng-shou HU
    2009, 29(1):  69-73. 
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    Objective: This study was designed to investigate the retainage rate, distribution, and emigration of the bone marrow mesenchymal stem cell (BMMSC) after transcoronary infusion and further evaluate the feasibility of BMMSCs injected into coronary artery. Method: BMMSCs were isolated, purified, expanded, and labelled with CM-DiI. In vitro study, the infarcted SD rat hearts were removed and perfused with Langendorff apparatus. The cells were injected into the aortic root and the fluid returning from the coronary system was collected and the labelled cells in the coronary effluent were quantitated with flowcytometry. At the same time left ventricle function was recorded to evaluate the safety of this approach. In vivo study, the cells were then injected into the briefly distally clamped ascending aorta through a catheter inserted through the left ventricle into the aortic root. The hearts were harvested at different time points after cell transplantation to obtain the direct evidence of distribution and emigration of the implanted cells. Results:In vitro study, we found that only 3-5% of transplanted cells returned into the right ventricle and more than 90% cells retained in the heart after injecting into the aortic root of Langendorff model of infarcted hearts of SD rats. Left ventricle function did not deteriorate after cell transplantation. In vivo study, the labelled cells were entrapped within the coronary capillary immediately after cell infusion, mainly in the normal area. After 24 hours some cells migrated through the capillary wall into interstitium of the heart. After 1 week later we could found that most survival cells located at the infarcted area and the border zone. Conclusion: The majority of BMMSCs delivered by transcoronary infusion retained in the heart. BMMSCs could cross the vessel wall and home to the interstitial compartment and the injured area in a few hours.
    Estrogen down-regulated the expression of high mobility group box 1 in human breast cancer cell line MCF-7
    Ru-jun GU; Dong-liang LIU; Yun MA; Wei WANG
    2009, 29(1):  74-77. 
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    Objective To investigate the effects of estrogen and tamoxifen on the expression of high mobility group box 1 (HMGB1) in human breast cancer cell line MCF-7. Methods MCF-7 cells were incubated with 17-beta E2 and tamoxifen at different concentrations for 4 d, respectively, with absolute ethanol as negative control. Real time RT-PCR and Western blotting were used afterward to detect the expression of HMGB1 at mRNA and protein level after different treatment to the cell line, respectively. Results Compared with ethanol control, HMGB1 mRNA and protein levels were significantly decreased when 17-beta-E2 was added at concentrations of 10-6 and 10-4 mol/L (P<0.05). And HMGB1 expression was significantly increased when tamoxifen was added at concentrations of 10-6 and 10-4 mol/L (P<0.05). Conclusion Estrogen could down-regulate the expression of HMGB1, while its antagonist tamoxifen has an opposite effect. So, HMGB1 probably has an inhibitory effect on breast neoplasms proliferation.
    技术与方法
    Convenient and Efficient Cultivation of HUVECs
    Jing LU; Jun ZHAO; Hong-yan YANG; You-tian HUANG; Zhi-min ZHENG; Ming-yao ZHAO; Zi-ming DONG
    2009, 29(1):  78-81. 
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    Objective To establish the convenient and efficient cultivation of HUVECs in vitro,so as to provide good seed cells for tissue engineering vascular grafts and related basic medical study. Methods 0.25%Trypsin perfusion method was used to isolate HUVECs,then cultivated in endothelial cell medium(ECM),identified the bionomics of HUVECs by checking Von Willebrand factor (VWF)、CD144 through immunocytochemical method and RT-PCR. HUVECs were suspended in cryopreserving solution containing with 10% glycerine and cryopreserved in liquid nitrogen for 4 weeks. The expression of CD144 and VWF of post-thawed cells were evaluated by Western blot. Results HUVECs grew to monolayer after cultivation for 2~3 days. They presented fusiform and appeared like Whirlpool under the light microscope, and presented lumens structure by passage,highly expressed VWF and CD144. The post-thawed cells maintained high proliferational ability and highly expressed VWF and CD144.Conclusion A large number of high purified HUVECs could be acquired by digestion of trypsin and cultivation of ECM,which could be good source cells for related study.
    Reference Genes Selection in mRNA Analysis for Aging Rat Tissues
    Wen-jing YE; Xiao-min ZHAO; Pei-qiang HOU; Hong-xin CAI; Zuo-li XIA
    2009, 29(1):  82-84. 
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    Objective To investigate the proper inner control genes suitable for mRNA expression level comparison of aging rat tissues. Methods Real-time reverse transcription PCR was used to examine in aging rat tissues the expression level of G3pd(glyceraldehyde-3-phosphate dehydrogenase),ACTB(?-actin),H3f3b(H3 histone, family 3B),Arbp(acidic ribosomal phosphoprotein P0)and 18S(18S ribosomal RNA ).Results The most stably expressed housekeeping gene in aging rat kidney was ACTB, as for heart and lung G3pd showed the minimum variation; Arbp expression was the most stable among different tissues. Conclusion For aging rat intra-tissue mRNA normalization at least two housekeeping genes should be used: one is the ribosomal RNA gene 18S and the other suitable control gene is Arbp.
    研究短文
    The enhancing effects of Norepinephrine on immune functions of rat peritoneal macrophages
    Jian-yun ZHOU; Jun YAN; Ce YANG; Qing LIU; Ying CHENG; Jian-xin JIANG
    2009, 29(1):  85-86. 
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    Changes of plasma adrenomedullin and endothelin-1 in patients with coronary artery bypass grafting
    Guang-qing CAO; Shu-ming WU; Xi-quan ZHANG; Yong-mei WANG; Min ZHOU; Rui-fang LIU; Shan-shan DUAN
    2009, 29(1):  87-88. 
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    Endogenous Carbon Monoxide Inhibits Vascular Tension Of Renal Hypertensive Rats
    Dong-wei PANG; Li HAN; Tie-min MA; Gui-lan PAN; Hai XU
    2009, 29(1):  91-92. 
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    短篇综述
    Research progress of stem cells in planarians
    Song-tao WANG; Guang-wen CHEN; Cun-shuan XU; Jing-bo ZHANG
    2009, 29(1):  93-96. 
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    The strong regenerative capacities of planarian have been considered to reside in a population of stem cells called the 'neoblasts'. These cells are the only mitotic cells in planarians, they play a great role in giving rise to the lost cells and reforming the missing structures. By the means of migrating, proliferating and differentiating of the neoblasts, any tiny amputated fragment of their body can regenerate into a complete individual. Advances in the study of stem cells in planarians are summered in this paper.
    Strategies for promoting survival, differentiation of stem cells after transplantation and repairing ischemic myocardium
    Xiao-jun CUI; Yu-zhen TAN; Hai-jie WANG
    2009, 29(1):  97-101. 
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    It is a key problem that the survival rate of stem cells is low in the ischemic myocardium microenvironment when treating ischemic diseases with stem cell transplantation. It is able to increase anti-apoptotic ability of the stem cells and promote their effective differentiation towards myocardial cells directly and indirectly by pretreating the stem cells with cytokines, drugs or chemical compounds, or modifying gene expression to promote cell adhesion, survival or angiogenesis for repairing ischemic myocardium and improving heart function after transplantation of the stem cells.
    Oncogene-induced Cellular Senenscence
    Ling ZHAO; Zhao-hui LU Jie CHEN
    2009, 29(1):  102-105. 
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    Oncogene-induced senenscence (OIS) is defined as a stable proliferative arrest of normal cells upon overexpression of aberrant proliferative signals of oncogenes through MAPK and PI3K pathway. The molecular mechanism of OIS is associated with the formation of heterochromatin and DNA-damage check-point response. The markers of OIS including senescence-associated β-galactosidase and senescence-associated heterochromatin foci. With the growing recognization of OIS, the new models of tumor progression are emerging. The further investigations of the mechanism of OIS are of great significance to our understanding of the tumorigenesis and provide new ideas and methods of cancer treatment.
    Focal Adhesion Kinase and Fibrosis
    Zhi-na DUN; Xiao-lan ZHANG
    2009, 29(1):  106-108. 
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    Focal adhesion kinase (FAK), a non-receptor protein tyrosine kinase, is at the cross of the numerous intra-cellular signal transduction. The activated FAK has been implicated in a diverse array of cellular behavious. Advanced relevant observations of FAK and fibrosis show that FAK plays an important role in fibrosis disease, the targeting of FAK may represents a novel therapeutic strategy.