共查询到20条相似文献，搜索用时 93 毫秒
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AIM: To explore interaction and biological behaviour changes of two kinds of cells-blastocysts and hepatocarcinoma cells in the same microenvironment. METHODS:The models of mouse blastocysts co-cultured with human hepatocarcinoma cell lines were established, then biological behaviours and mutual effects of the two kinds of cells in co-culture system were observed. RESULTS: Compared with control group, hepatocarcinoma cells with differently invasive and metastatic potential significantly enhanced the rates of blastocyst hatchment , attachment and outgrowth(P＜0.05). There was no significant difference in those among hepatocarcinoma cells co-cultured groups (P＞0.05). The blastocyst hatched and attached to hepatocarcinoma cells with differently invasive and metastatic potential. Then, differential trophoblasts invaded hepatocarcinoma cells. The clear-cut interfaces were gradually formed between both sides. Hepatocarcinoma cells on interface showed changes of growth direction and cell shapes and did not invade blastocysts. CONCLUSIONS: Hepatocarcinoma cells promoted blastocyst development. Blastocysts implanted and invaded hepatocarcinoma cells with differently invasive and metastatic potential in vitro, which indicate that blastocyst implantation in vitro does not relate with the kinds and differential level of interactional cells and the low selectivity maybe relate with high adaptability of early life. 相似文献
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HAN Li-hui SUN Wen-sheng LIU Su-xia JIA Xiao-qing WANG Xiao-yan MA Chun-hong GAO Li-fen ZHANG Li-ning CAO Ying-lin 《园艺学报》2005,21(8):1486-1490
AIM: To explore the effect of TNF-related apoptosis inducing ligand (TRAIL), a new apoptotic inducing molecule on the biological activity of hepatocarcinoma cell line. METHODS: The expression of membrane binding TRAIL on HepG2 cells was detected by immuno-cytochemistry. Quantity of secretory TRAIL was assayed by ELISA method. The cytotoxicity and apoptosis induced by TRAIL was detected by MTT and TUNEL method, respectively. The telomerase activity of HepG2 cells was detected by TRAP-PCR assay kit. The expression of hTERT, the catalytic subunit of telomerase, was detected by FCM. RESULTS: TRAIL was constitutively expressed on the membrane of HepG2 cell line. Soluble TRAIL was also expressed to a certain degree. Cytotoxicity assay showed that TRAIL significantly inhibited the growth of hepatocarcinoma cells. TUNEL assay indicated that TRAIL induced apoptosis in hepatocarcinoma cells. Detection of telomerase activity showed that TRAIL inhibited telomerase activity and the expression of telomerase catalytic subunit. CONCLUSION: TRAIL is an effective molecule to inhibit the growth of hepatocarcinoma through multiple pathways, such as inducing apoptosis and inhibiting the activity of telomerase. 相似文献
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YANG Xia WANG Qing-song CHENG Rui LI Chao-yang CAI Wei-bin YANG Zhong-han LI Min-you HE Guang-yao GAO Guo-quan 《园艺学报》2008,35(2):220-224
AIM:To investigate the effects of plasminogen kringle 5(K5) deletion mutantⅠ(K5 mut1) on the neovascularization and growth of hepatocarcinoma in vivo. METHODS:K5 mut1 was expressed in E. coli BL-21(DE3) induced by IPTG and purified by Ni2+-His Bind Resin affinity chromatography. The purity and identity of K5 mut1 was examined by SDS-PAGE and Western blotting analysis. K5 mut1 activity was evaluated in vivo, HepA-grafed hepatocarcinoma mouse model was established by subcutaneously injection of mouse hepatoma cells(1×106) into the oxter of mice, and the mice were then divided into different groups and treated with PBS and K5 mut1 at different doses, respectively. The tumor suppressing rate and micro vascular density (MVD) in hepatoma tissues were assayed. RESULTS:The purity of recombinant K5 mut1 was over 90% according to the analysis of SDS-PAGE and Western blotting analysis. K5 mut1 significantly inhibited the growth of tumor in a HepA-grafed hepatocarcinoma mouse model and decreased microvessel density (MVD) in hepatoma tissues in a dose-dependent manner, compared with PBS control group. CONCLUSION:K5 mut1 exhibits anti-tumor effect in a HepA-grafted hepatocarcinoma mice model by the anti-angiogenic activity. These results support the conclusion that K5 mut1 may be a promising angiogenesis inhibitor and tumor suppressor with considerable therapeutic potential in liver cancer. 相似文献
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ZHENG Qing WANG Xiao-feng WU Xiao-ping XU Hua ZHANG Qi-hao SU Zhi-jian LI Xiao-kun 《园艺学报》2005,21(3):446-448
AIM: To observe the effects of the human acidic fibroblast growth factor mutant (mhaFGF)， lacking 27 amino acids at N-terminal， on the proliferation and signal transduction of the hepatocarcinoma cells. METHODS: The hepatocarcinoma cells were treated with human acidic fibroblast growth factor (haFGF) and mhaFGF, respectively. The expression levels of the signal proteins, Grb2 and Erk1/2, in the hepatocarcinoma cells were detected by semi-quantitative Western-blotting after treated for 15 min. The mitogenic activity of both haFGF and mhaFGF was detected by MTT method and the cell cycle was analysed by flow cytometer (FCM) after treated for 48 h. RESULTS: The mitogenic activity and the ratio of G1 and S phase cells in mhaFGF-treated cells were markedly lower than that of the haFGF, and close to that of the control group. The expression level of both Grb2 and Erk1/2 in the mhaFGF-treated cells were lower than those in the haFGF- treated cells. CONCLUSION: The decrease in the mitogenic activity of mhaFGF is probably associated to its down-regulating the expression of the signal molecular, MAPK-ERK1/2 and Grb2. 相似文献
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AIM: To investigate the effect of Sonic Hedgehog (Shh) signaling blockade on the growth of hematocarcinoma cells and underlying mechanisms. METHODS: The expression of Shh signaling molecules in hematocarcinoma cell lines BEL-7402, Huh7 and HepG2 was detected by RT-PCR. The cell viability was detected by MTT assay. The cell cycle and apoptosis were analyzed by flow cytometry. The expression of apoptosis-related proteins was determined by Western blot. RESULTS: Shh signaling molecules were all expressed in BEL-7402, Huh7 and HepG2 cells. The mRNA expression of Patched (Ptch), Gli1 and Gli2 was down-regulated by anti-Shh antibody. Blockade of Shh signaling pathway inhibited the proliferation of hepatocarcinoma cells with increasing cells in G0/G1 phase and induced the apoptosis of hepatocarcinoma cells. Treatment with anti-Shh antibody down-regulated the protein expression of pro-caspase-3, pro-caspase-8 and pro-caspase-9, while up-regulated the protein levels of cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9 in BEL-7402 cells. CONCLUSION: Blockade of Shh signaling pathway inhibits the growth of hepatocarcinoma at different levels by cell cycle arrest and inducing apoptosis of hematocarcinoma cells. 相似文献
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AIM: To explore the different inhibitory effect of arsenic trioxide (As2O3) on hepatocarcinoma cell growth in SMMC-7721 and BEL-7402 cell lines and its mechanism. METHODS: The cell culture and trypan blue staining were used to study the inhibitory effect of arsenic trioxide on cell growth, and the glutathione (GSH) contents in hepatocarcinoma cells treated with arsenic trioxide were detected. RESULTS: Arsenic trioxide inhibited the growth of BEL-7402 cells in a time and dose-dependent manner. The inhibitory effect was significant at a lower dose of 0.50 μmol/L for 24 h, however, to SMMC-7721 cells, a higher dose of 2.00 μmol/L for 96 h was needed. The inhibitory rate of arsenic trioxide (0.25-2.00 μmol/L) on BEL-7402 cell growth was higher than that on SMMC-7721 cells. The content of GSH in SMMC-7721 cells was much higher than that in BEL-7402 cells . CONCLUSION: There was a significant difference in inhibition of hepatocarcinoma cell growth by arsenic trioxide between BEL-7402 and SMMC-7721 cell lines, the cause of which may be due to the difference in GSH content in BEL-7402 and SMMC-7721 cells. 相似文献
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AIM：To investigate the effect of microRNA-100 (miR-100) on the proliferation activity and cell cycle of hepatocarcinoma cells. METHODS：Synthetic miR-100 mimic and its negative control were transfected into human hepatocarcinoma HepG2 cells by liposome method. After transfection, the cell counting kit-8 (CCK-8) was used to measure the cell proliferation activity. The cell cycle distribution was determined by flow cytometry. The expression of Polo-like kinase 1 (Plk1) at mRNA and protein levels was detected by quantitative real-time PCR (qRT-PCR) and Western blotting. RESULTS：The transfection efficiency mediated by cationic liposome was greater than 85%. The inhibitory rates of cell proliferation in HepG2 cells were (43.5±12.2)%, (46.5±3.7)% and (52.1±0.2)% at 24 h, 48 h and 72 h after transfected with miR-100 mimic, respectively, which were significantly increased as compared with the control cells. Moreover, the cell proliferation index in experimental group (35.8 ± 1.4) was higher than that in negative control group (39.2 ± 1.0) and simple liposome group (40.7 ± 2.0) at 72 h. At the same time, the mRNA and protein expression levels of Plk1 obviously decreased in HepG2 cells transfected with miR-100 at 72 h after transfection. CONCLUSION：miR-100 suppresses the proliferation activity of hepatocarcinoma cells by down-regulating Plk1 gene expression. 相似文献
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LIU You-ping LI Juan DAI Rong-yang DUAN Chun-yan CHEN Shao-kun YAN Dong-mei CHEN Chuan-ning LI Hong 《园艺学报》2011,27(2):367
AIM: To determine whether microRNA-26a(miR-26a) is involved in development of liver cancer by analysis of proteomic expression profile of human hepatocarcinoma cell HepG2 transfected with miR-26a mimics.METHODS: HepG2 cells were cultured by a routine method and transfected with miR-26a mimics for 48 h for cell cycle analysis. The expressive proteome profiles of HepG2 cells with or without miR-26a mimics treatment were established by the methods of two-dimensional electrophoresis separation following lysis of the cells and extraction of the proteins. The proteomic expression profiles were analyzed by comparative proteomics technique to discover the important protein spots with differential expression. The identification of the proteins was conducted by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry(MALDI-TOF-MS). RESULTS: miR-26a brought down the proliferation of HepG2 cells. Total 11 protein spots with alteration of expressive amounts more than 2 times were successfully identified in the proteomic expression profile of HepG2 cells treated with miR-26a mimics, including annexin A1, peroxiredoxin 4, proliferating cell nuclear antigen, apolipoprotein A1, cytochrome C oxidase subunit 5A, cyclin E2, ribose-phosphate pyrophosphokinase 3, cyclin-dependent kinase 1 and phosphatidylethanolamine-binding protein 1. Among these, the expression of 3 protein spots was up-regulated and 8 of them was down-regulated.CONCLUSION: miR-26a contributes to the anti-cancer effect by expressive regulation of the proteins mentioned above, or directly or indirectly controls the proliferation, differentiation and death of hepatocarcinoma cells. 相似文献
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AIM: To investigate the expression of microRNA-141 (miR-141) in human hepatocellular carcinoma (HCC) cell line SMMC-7721 and normal hepatocyte line HL-7702, and to analyze the effect of abnormal expression of miR-141 on the malignant biological behaviors of human hepatocarcinoma cells. METHODS: The RNA from SMMC-7721 cells and HL-7702 cells was extracted. SYBR Green real-time PCR was performed to detect the expression of miR-141. Synthetic miR-141 mimic and its negative control were transfected into the SMMC-7721 cells, and miR-141 inhibitor and its negative control were transfected into the HL-7702 cells by the method of Lipofectamine. After transfection, MTS assay and BrdU-ELISA were employed to evaluate the effect of miR-141 on the cell proliferation. Flow cytometry was used to detect cell cycle and apoptosis. The changes of migration ability were investigated by Transwell invasion assay. RESULTS: The expression of miR-141 in the SMMC-7721 cells was significantly lower than that in the HL-7702 cells (P < 0.05). Compared with blank group, Lipofectamine group and negative control group, the proliferation of the SMMC-7721 cells transfected with 25 nmol/L miR-141 mimic was significantly inhibited in a time-dependent manner (P < 0.05). The percentages of G1 phase cells and early apoptotic rate were significantly increased when miR-141 was up-regulated, but the migration ability was inhibited (P < 0.05). Compared with blank group, Lipofectamine group and negative control group, the proliferation of HL-7702 cells transfected with 50 nmol/L miR-141 inhibitor was significantly increased in a time-dependent manner (P < 0.05). When miR-141 was down-regulated, the percentages of G1 phase cells and early apoptotic rate were significantly decreased, but the migration ability was enhanced (P < 0.05). CONCLUSION: miR-141 is down-regulated in human hepatocarcinoma cell line. Up-regulation of miR-141 will not only inhibit cell proliferation and migration ability, but also affect the cell cycle and apoptosis of SMMC-7721 cells. miR-141 may function as a tumor suppressor gene during HCC development. 相似文献
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WANG Hua ZHOU Bin GUO Xing ZHU Jun-ya CHENG Chun ZHU Chang-lai ZHANG Tian-yi 《园艺学报》2011,27(6):1226-1229
AIM: To investigate the changes of cell growth and cytoskeleton in hepatocarcinoma SMMC-7721 cells treated with ginsenoside Rh2.METHODS: Cell viability and apoptosis under the conditions of ginsenoside Rh2 exposure at different concentrations were measured by MTT test and flow cytometry,respectively. The morphological changes of F-actin labeled with FITC-phalloidin were observed under confocal laser scanning microscope. The structures of nuclear matrix-intermediate fibre system were observed under transmission electron microscope (TEM).RESULTS: Rh2 at 40 mg/L for 4 days inhibited the proliferation and induced apoptosis in SMMC-7721 cells more than those in control group, 10 mg/L Rh2 group and 20 mg/L Rh2 group. The F-actin in the cells treated with Rh2 was well-distributed, lined up in order and the number of fibers increased, while those in the control cells were in disorder and punctiform. The results of whole mount TEM indicated that the intermediate fiber was plentiful, well-distributed and interweaved into a regular network in Rh2 treated cells.CONCLUSION: Rh2 effectively inhibits the cell proliferation, increases the cell apoptosis and induces the change of the cytoskeleton alignment in SMMC-7721 cells. 相似文献
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AIM: To investigate the proliferation-inhibitory and apoptosis-inducing effects of harmine on human hepatocarcinoma HepG2 cells. METHODS: The proliferation of HepG2 cells was determined in the absence or presence of a JNK inhibitor SP600125 by Cell Counting Kit-8 (CCK-8) assay and colony formation test. The morphology of HepG2 cells was observed by Hoechst 33258 staining under fluorescence microscope. The cell apoptosis was analyzed by Annexin V-PI staining. The expression of apoptosis-regulated proteins,poly(ADP-ribose) polymerase (PARP),c-Jun N-terminal kinase (JNK) and p-JNK, was detected by Western blotting. The sensitizing effects of harmine on HepG2 cells to chemotherapeutic drugs 5-fluorouracil (5-FU) and cisplatin were determined by CCK-8 assay. RESULTS: Harmine inhibited the proliferation of HepG2 cells and induced apoptosis in a dose-dependent manner. After the JNK signaling pathway was blocked by SP600125, the cell apoptotic rate decreased significantly. Hoechst 33258 staining revealed that the nuclear fragmentation, chromosomal condensation, cell shrinkage and attachment loss appeared in the HepG2 cells treated with harmine. The percentage of the sub-G1 fraction was increased and the population of early apoptotic cell death was observed. Apoptosis of HepG2 cells with harmine treatment was associated with the activation of JNK. Combined with harmine, the IC50 values of 5-FU and cisplatin for the tumor cells were 1.47 and 5.78 times sensitized as compared with the correspon-ding single drug treatment groups, respectively. CONCLUSION: Harmine exhibits an anti-proliferative effect on HepG2 cells by inducing apoptosis. The JNK signaling pathway is involved in the apoptosis of HepG2 cells. Harmine enhances the chemosensitivity of the cells to 5-FU and cisplatin. 相似文献
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CHEN Kun CHEN Yong-shun WANG Xue-jun CHEN Yun-fan LIU Ke-li CHEN Feng-jia LU Jian-jun 《园艺学报》2014,30(3):385-393
AIM：To investigate the effect of ethyl docosahexaenoate (Et-DHA) on the apoptosis of human hepatocarcinoma HepG2 cells. METHODS：HepG2 cells were used to test the anticarcinogenicity of Et-DHA. The direct inhibition of HepG2 cells by Et-DHA was detected by MTT. Nuclear morphological features of the HepG2 cells were observed under fluorescence microscope after staining with Hochest 33258. The levels of Bax, Bak, Bid, Bcl-2, Smac and cytochrome C (Cyt C) in mitochondria and cytosol, the cleaved caspase-8, cleaved caspase-9, and cleaved caspase-3 in cytosol, as well as the release of reactive oxygen species (ROS), total superoxide dismutase (SOD) and caspase-9 activity in the Et-DHA-treated HepG2 cells were determined by Western blotting and ELISA. Furthermore, by co-culturing the HepG2 cells with T cells, the effects of proliferation of Et-DHA-treated T cells on the activity of HepG2 cells were observed, and the level of granzyme B was detected. RESULTS：Et-DHA significantly inhibited the growth of HepG2 cells in a concentration- and time-dependent manner. The ROS release and caspase-9 activity increased markedly in Et-DHA-treated HepG2 cells, and no significant change of the total SOD activity was observed. The levels of the pro-apoptotic proteins Bax, Bak and Bid in mitochondria increased, the anti-apoptotic protein Bcl-2 as well as mitochondrial Cyt C and Smac levels decreased, and the cytoplasmic Cyt C, Smac, cleaved caspase-8, cleaved caspase-9, cleaved caspase-3 and cleaved Bid levels showed dose-dependent increases. Additionally, the degree of Et-DHA-induced apoptosis in HepG2 cells in the co-culture group (T cells+HepG2 cells) showed a further increase as compared with the HepG2 cells treated with Et-DHA alone. Due to Et-DHA inducing elevation of granzyme B level in the T cells, the granzyme B released into HepG2 cells was significantly increased. CONCLUSION:Et-DHA might induce the apoptosis of HepG2 cells through activation of caspase-3 mainly via a mitochondrial intrinsic pathway and a caspase-8 pathway, and promote the increase in granzyme B indirectly by activating T cells, thus enhancing the cytotoxic effect on HepG2 cells. 相似文献
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Artificial joint replacement is an important operation to treat end-stage joint diseases. However, aseptic loosening after artificial joint replacement is the main cause of joint renovation. In this paper, we review the etiological factors of aseptic loosening after artificial joint replacement and analyze the pathogenesis of this process. Four factors of aseptic loosening are included: prosthesis material and installation, mechanical factor, wear particle and inflammation, and other possible factors. These etiological factors are analyzed and summarized in order to provide reference for the diagnosis and treatment. 相似文献
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蔷薇科果树在世界果品生产中占据重要地位。近年来,蔷薇科果树离体再生和遗传转化研究取得了较大进展,在较大的树种上均有报道,但对于离体再生与遗传转化体系的主要影响因素和技术参数细节等缺少系统总结。从离体再生途径、离体再生影响因素、遗传转化概况、农杆菌介导的遗传转化体系影响因素等方面进行了重点总结,对未来研究趋势和热点进行了展望。 相似文献
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果蔬采后叶绿素降解与品质变化的关系 总被引：16，自引：1，他引：15
介绍了叶绿素降解的研究进展、果蔬采后叶绿素降解与品质变化的关系、影响果蔬采后叶绿素降解的因素以及相关采后贮藏技术措施。相对于叶绿素的合成,叶绿素降解的研究进展要缓慢得多。目前认为,叶绿素在绿色植物和成熟果实中的降解,至少有2条途径。一是包括叶绿素酶等在内的“PaO”途径降解;另一条是由一系列的氧化酶作用的叶绿素“漂白”过程。在果实以及蔬菜的采后贮藏中,有许多因素影响着叶绿素的降解,如温度、气体条件、植物激素等。在广泛研究了叶绿素降解影响因素的基础上,根据果实的采后生理特点以及市场对产品的要求,研究出了如热处理、气调控制、药物处理等技术,从而有效地控制了果蔬采后叶绿素的降解,以满足市场与消费者的要求,同时也为更多技术的出现奠定了基础。 相似文献
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The intermediate phenotype of vascular smooth muscle cell in adult is the dedifferentiation state returned from the high differentiation state, appeared on the damaged blood vessels.It is regulated by many factors.Its distribution, the characteristics of morphology and structure, the regulated transform factors and the molecular biological mechanism are introduced, and its functional significance and the role in vascular diseases are also discussed in this article. 相似文献