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目的探讨油橄榄叶提取物(OLE)对铅中毒小鼠胸腺的影响.方法选健康小鼠,每日灌胃醋酸铅溶液的同时灌胃不同剂量的OLE进行治疗,连续用药30d,检测胸腺指数、胸腺T细胞亚群、胸腺细胞凋亡率及胸腺细胞周期进程的变化情况.结果与模型对照组相比,小鼠灌胃OLE后胸腺指数明显升高,胸腺细胞亚群CD8标记率明显降低,胸腺细胞周期进程中G2+M期细胞百分比升高,胸腺细胞凋亡率明显降低.结论 OLE对铅中毒小鼠有一定的疗效,能抑制胸腺细胞凋亡,影响胸腺细胞周期进程,拮抗铅对胸腺的毒性. 相似文献
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淋巴样前体细胞由CD4-CD8-双阴性细胞发育为CD4 CD8 双阳性细胞,经历阳性选择和阴性选择进一步分化发育为具有免疫功能的成熟T细胞,即CD4 Th和CD8 Tc。T细胞发育的这一过程需要准确的调控机制,Hedgehog,BMP和Wnt信号通路参与了T细胞发育过程的调控。Hedgehog信号和BMP信号抑制T细胞的增殖和分化,Wnt信号对T细胞的发育起正调控作用。 相似文献
3.
Caspase与细胞凋亡 总被引：2，自引：0，他引：2
兰栋 《岳阳职业技术学院学报》2009,24(1)
细胞凋亡是不同于细胞坏死的生理性死亡方式,对生物机体的正常发育及自身稳定具有极其重要的作用.细胞凋亡的失控可以引起生物体平衡失调,导致各种相关疾病的发生.细胞凋亡的过程非常复杂,caspase家族对细胞的调控起着举足轻重的作用,与疾病的发生关系密切. 相似文献
4.
目的 :研究新城疫病毒在体外抗胃癌细胞活性及其与细胞凋亡的关系。方法 :应用倒置显微镜观察细胞形态、MTT法测NDV在体外对BGC - 82 3的抑制和杀伤作用 ,同时用流式细胞术检测胃癌细胞凋亡情况及细胞分裂周期各时象的变化。结果 :NDV在体外可使BGC - 82 3胃癌细胞形成明显的细胞病变效应、细胞生长抑制及细胞凋亡 ,且细胞凋亡率与感染时间呈正相关。G2、S期细胞减少 ,增殖指数 (PI)降低 ,与阴性对照组比较有显著性差异 (P<0 .0 1)。结论 :NDV具有显著的抗BGC - 82 3胃癌细胞活性。 相似文献
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细胞凋亡是细胞的主动死亡过程,涉及一系列基因的表达和调控。在细胞的正常发育过程中,约有半数细胞通过凋亡途径被清除。凋亡蛋白酶在细胞凋亡中具有不同功能,可以将其分为两类：第一类直接对细胞的功能蛋白进行水解并导致细胞解体,称为效应凋亡蛋白酶;第二类参与上游事件的调节并启动蛋白酶解级联反应,称为启动凋亡蛋白酶。在细胞凋亡过程中,作为传感器的细胞表面凋亡受体接受由凋亡配体发出的凋亡信号,并传递到胞内,激活凋亡蛋白酶家族成员,借助凋亡信号结构域相继激活凋亡蛋白酶,进而降解特定的靶蛋白,最终导致细胞死亡。 相似文献
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张海英 《赤峰学院学报(自然科学版)》2008,(9)
细胞凋亡是不同于细胞坏死的生理性细胞程序化死亡,它涉及到生命科学的各个领域,与运动医学的关系也非常密切,笔者综述了运动对骨骼肌、心肌、肝细胞和脑细胞凋亡的影响及其调节机制,旨在为进一步研究运动性疲劳的发生机制开辟一条新的途径. 相似文献
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Th17细胞和Treg细胞是CD4+T细胞的新亚群,在分化发育、功能发挥的过程中受到Th1型、Th2型效应细胞以及自身分泌产生的细胞因子的调节,参与自身免疫、感染、肿瘤等疾病的发生发展.Th17/Treg细胞失衡在许多免疫性疾病的发病机制中发挥重要作用.通过对Th17和Treg分化发育和功能发挥过程中的关键调节因子进行阻断或加强,可以上调或下调Th17细胞和Treg细胞在疾病中的表达,以用于疾病的预防和诊治. 相似文献
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紫草素及其衍生物是中药紫草的有效化学成份，文章对紫草素抗肿瘤作用及其机制的研究作一综述。紫草素能抑制多种肿瘤细胞生长增殖，致肿瘤细胞凋亡，其作用机制包括：调节MAPK信号通路、引起Bcl-2蛋白家族表达变化从而促进细胞色素c的释放、激活Caspase蛋白酶家族启动凋亡、致肿瘤细胞周期阻滞、影响死亡受体家族及其相关蛋白活性等方面。动物实验和临床观察表明：紫草素具有较强的抑癌作用，对正常细胞毒副作用小。 相似文献
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金银花无性快速繁育技术具有广阔的发展前景.本文阐述了组织培养的外植体、初代培养、增殖培养、生根培养、炼苗与移栽管理以及扦插繁殖的育苗地选择、扦插时间、插条选择与处理、扦插后管理,对金银花无性快速繁育技术起到一定的指导作用. 相似文献
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Homoharringtonine (HHT) has currently been used successfully in the treatment of acute and chronic myeloid leukemias and has been shown to induce apoptosis of different types of leukemic cells in vitro. Emerging evidence suggests that angiogenesis may play an important role in hematological malignancies, such as leukemia. How ever, whether HHT can relieve leukemia by anti-angiogenesis is still unknown. We investigated the anti-angiogenesis potential of HHT with the human umbilical vein endothelial cell line (ECV304) and leukemic cell line (K562) in vitro. Cellular proliferation was determined by MTT assay and apoptosis was analyzed by flow cytometry. The mRNA expression of vascular endothelial growth factor (VEGF) was assessed by RT-PCR and VEGF protein production was detected by Western blot. Inhibition of cell proliferation and induction of apoptosis by HHT were discovered in ECV304 cells, and appeared in a dose- and time-dependent manner. Also, treatment with HHT caused down-regulation of VEGF mRNA expression in K562 cells in similar dose- and time-dependent manner and inhibition of VEGF protein production in K562 cells in response to the enhancing concentration of HHT. The results demonstrated that HHT could also induce apoptosis in endothelium and down-regulate VEGF expression in K562 cells. In conclusion, we believe HHT has anti-angiogenesis potential and speculate that HHT might exert its anti-leukemia effects via reduction of angiogenesis. 相似文献
13.
Homoharringtonine induces apoptosis of endothelium and down-regulates VEGF expression of K562 cells 总被引：1，自引：0，他引：1
INTRODUCTION Homoharringtonine (HHT) is a cephalotoxin alkaloid with anti-leukemic activity and had been used successfully in the treatment of acute and chronic myeloid leukemias (O払rien et al., 1995; 1999; Feldman et al., 1992). The principal mecha-nism of action by HHT is the inhibition of protein synthesis in a dose- and time-dependent manner by binding to ribosome and inhibiting polypeptide chain elongation (Tujebajeva et al., 1989; Zhou et al., 1995). HHT had been shown to indu… 相似文献
14.
The development of ovarian follicular cells is controlled by multiple circulating and local hormones and factors, including
follicle-stimulating hormone (FSH) and epidermal growth factor (EGF). In this study, the stage-specific effect of EGF on FSH-induced
proliferation of granulosa cells was evaluated in the ovarian follicles of egg-laying chickens. Results showed that EGF and its receptor (EGFR) mRNAs displayed a high expression in granulosa cells from the prehierarchical follicles, including the large white follicle
(LWF) and small yellow follicle (SYF), and thereafter the expression decreased markedly to the stage of the largest preovulatory
follicle. SYF represents a turning point of EGF/EGFR mRNA expression during follicle selection. Subsequently the granulosa cells from SYF were cultured to reveal the mediation
of EGF in FSH action. Cell proliferation was remarkably increased by treatment with either EGF or FSH (0.1–100 ng/ml). This
result was confirmed by elevated proliferating cell nuclear antigen (PCNA) expression and decreased cell apoptosis. Furthermore,
EGF-induced cell proliferation was accompanied by increased mRNA expressions of EGFR, FSH receptor, and the cell cycle-regulating
genes (cyclins D1 and E1, cyclin-dependent kinases 2 and 6) as well as decreased expression of luteinizing hormone receptor
mRNA. However, the EGF or FSH-elicited effect was reversed by simultaneous treatment with an EGFR inhibitor AG1478. In conclusion,
EGF and EGFR expressions manifested stage-specific changes during follicular development and EGF mediated FSH-induced cell
proliferation and retarded cell differentiation in the prehierarchical follicles. These expressions thus stimulated follicular
growth before selection in the egg-laying chicken. 相似文献
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目的探讨银杏叶总黄酮对体外培养的人肝癌细胞HepG2增殖与凋亡的影响。方法将银杏叶总黄酮作用于体外培养的人肝癌细胞HepG2,MTT法检测其对HepG2细胞增殖的影响,缺口末端核苷标记（TUNNEL）法检测其对HepG2细胞凋亡的影响。结果银杏叶总黄酮对体外培养的人肝癌细胞HepG2的增殖效率下降,使凋亡细胞数增加（P〈0．01）,且呈剂量依赖效应。结论银杏叶总黄酮对体外培养的人HepG2细胞增殖有抑制作用,并能诱导细胞凋亡。 相似文献
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研究了没食子儿茶素没食子酸酯（EGCG）对人肝癌细胞BEL-7402增殖凋亡及对信号转导蛋白和转录激活因子3（Stat3）蛋白及磷酸化Stat3蛋白表达的影响.应用MTT法检测不同浓度EGCG对BEL-7402细胞增殖的抑制作用,用流式细胞仪分析细胞的凋亡率,用ELISA方法检测EGCG对Stat3蛋白及磷酸化的Stat3蛋白表达的影响.结果表明：EGCG有抑制肝癌细胞增殖促进凋亡的作用,并呈剂量依赖性.ELISA结果显示EGCG能降低磷酸化Stat3蛋白的表达水平.EGCG能抑制肝癌细胞的增殖促进凋亡,其机制可能有与下调磷酸化的Stat3蛋白的表达有关. 相似文献
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目的探讨银杏叶黄酮单体成分槲皮素体外对人肝癌细胞HepG2增殖与凋亡的影响。方法将银杏叶黄酮单体成分槲皮素作用于体外培养的人肝癌细胞HepG2,MTT法检测其对HepG2细胞增殖的影响,缺口末端核苷标记（TUNNEL）法检测其对HepG2细胞凋亡的影响。结果银杏叶黄酮单体成分槲皮素使体外培养的人肝癌细胞HepG2的增殖效率下降,使凋亡细胞数增加（P〈0.01）,两者均呈剂量依赖效应。结论银杏叶黄酮单体成分槲皮素具有与银杏叶总黄酮相似的作用,对体外培养的人HepG2细胞增殖有抑制作用,并能诱导细胞凋亡。 相似文献
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This article is to summarize the molecular and functional analysis of the gene "suppression of tumorigenicity 13"(ST13). ST13 is in fact the gene encoding Hsp70 interacting protein (Hip), a co-factor (co-chaperone) of the 70-kDa heat shock proteins (Hsc/Hsp70). By collaborating with other positive co-factors such as Hsp40 and the Hsp70-Hsp90 organizing protein (Hop), or competing with negative co-factors such as Bc12-associated athanogen 1 (Bag1), Hip facilitates may facilitate the chaperone function of Hsc/Hsp70 in protein folding and repair, and in controlling the activity of regulatory proteins such as steroid receptors and regulators of proliferation or apoptosis. Although the nomenclature of ST13 implies a role in the suppression of tumorigenicity (ST), to date available experimental data are not sufficient to support its role in cancer development, except for the possible down-regulation of ST13 in gastric and colorectal cancers. Further investigation of this gene at the physiological level would benefit our understanding of diseases such as endocrinological disorders, cancer, and neurodegeneration commonly associated with protein misfolding. 相似文献
19.
杨杰 《安徽教育学院学报》2003,21(6):70-71
酒精对发育中的脑有严重的损伤作用，如通过阻断NMDA受体和过度激活GABA受体的双重机制，广泛地引起脑部神经元凋亡，消弱胰岛素刺激的小脑神经元存活，抑制齿状回中新细胞的形成并加速细胞凋亡，导致大脑海马区退化性的改变等。 相似文献
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Bo Wang Sheng-yun Lin Ying-ying Shen Li-qiang Wu Zhen-zhen Chen Jing Li Zhi Chen Wen-bin Qian Jian-ping Jiang 《Journal of Zhejiang University. Science. B》2015,16(7):580-585
To investigate the potential effects of pure total flavonoid compounds (PTFCs) from Citrus paradisi Macfadyen separately or combined with arsenic trioxide on the proliferation of human myeloid leukemia cells and the mechanisms underlying the action of PTFCs. The effects of PTFCs separately or combined with arsenic trioxide on the proliferation and apoptosis of leukemia cells were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), fluorescence microscopy, and flow cytometry. Their effects on the expression levels of apoptosis-related regulators were determined by Western blot assay. PTFCs combined with arsenic trioxide significantly inhibited the growth of Kasumi-1 cells, and apoptosis was confirmed by flow cytometry analysis. Hoechst 33258 staining showed more significant morphological changes and more apoptosis following the combined treatment. Western blots showed changes in the expression of genes for poly ADP-ribose polymerase (PARP), caspase 3/9, and P65. The results indicated that PTFCs separately or combined with arsenic trioxide inhibited proliferation of leukemia cells in vitro and induced their apoptosis by modulating the expression of apoptosis-related regulator genes. 相似文献