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1.
高中《生物》新课标教材“分子与细胞”中,一个较大的变化就是新增了细胞凋亡的知识点。由于教材中关于细胞凋亡的表述相对简单,给师生的理解带来了一定的难度,为了便于课堂教学,就细胞凋亡相关知识作补充阐述,以飨读。  相似文献   

2.
线粒体与细胞凋亡   总被引:5,自引:0,他引:5  
细胞编程性死亡即细胞凋亡是健康个体中的一个正常过程.近年来发现细胞凋亡与线粒体的结构与功能有着密切的关系.线粒体氧化磷酸化过程中生成活性氧,使线粒体上PT孔道开放,削弱了线粒体膜两侧的质子梯度,导致ATP合成下降;同时向细胞液释放了与凋亡有关的活性物质,激活Caspases,引起细胞凋亡.  相似文献   

3.
本简要介绍了病毒感染与细胞凋亡之间的相互关系,以及近年来在该方面研究所取得的部分进展,阐述了DNA病毒和RNA病毒诱导细胞凋亡方面所存在的显差异,初步探讨了病毒与其宿主细胞之间的复杂相互关系,病毒感染诱导凋亡的机制。  相似文献   

4.
细胞凋亡是新陈代谢过程中调节细胞数和生命活动的重要环节,现已明确各种肿瘤是细胞死亡失控的疾病,亦即凋亡受阻导致了细胞代谢紊乱及肿瘤的发生和发展,治疗肿瘤最有效的途径之一是直接诱导肿瘤细胞凋亡,现有许多研究证明三氧化二砷具有一个对较广的诱导凋亡效应谱。  相似文献   

5.
对细胞凋亡概念的认识   总被引:1,自引:0,他引:1  
综述了细胞死亡研究中出现的坏死、细胞凋亡、程序性细胞死亡、生理性细胞死亡、形态发生性死亡、细胞自杀等概念;着重讨论了细胞凋亡与程序性细胞死亡、细胞自杀之间关系,明确细胞死亡有两种模式:细胞凋亡和坏死。  相似文献   

6.
线粒体与细胞凋亡   总被引:2,自引:0,他引:2  
随着近年来对线粒体研究的深入,发现线粒体与细胞凋亡有着密切的关系。它通过释放细胞色素C、凋亡诱导因子AIF,或者通过产生氧自由基等多种途径导致细胞凋亡。  相似文献   

7.
细胞凋亡是细胞与生俱来的一种机制,是最常见的细胞生理性死亡形式。高浓度的活性氧是启动细胞凋亡的信号。它是在电子传给末端氧化酶之前漏出呼吸链与氧反应生成的。活性氧水平的升高使线粒体上非特异性的通透性转运孔道开放,于是原来位于线粒体膜间隙的某些与凋亡有关的活性物质释放到细胞液中,激活胱天蛋白酶,引起细胞凋亡。位于凋亡后期的效应因子也可被不同的凋亡前期信使分子所激活,而IAP蛋白则能通过直接抑制胱天蛋白酶家族蛋白的活化过程而抑制凋亡的发生。  相似文献   

8.
结合教材和相关文献,对细胞死亡、细胞凋亡和细胞自噬中的疑难知识进行了释疑,阐明细胞程序性死亡不仅仅有细胞凋亡,还包括细胞自噬;细胞凋亡、细胞自噬都与环境无关;细胞自噬不一定会促进细胞凋亡等疑难问题。  相似文献   

9.
本文介绍了细胞凋亡的概念及生物学特征,讨论了bcl-2、c-myc、P_(53)、Fas等相关基因在细胞凋亡中的作用,细胞凋亡在医学生物学中的意义,及细胞凋亡的研究方法。  相似文献   

10.
胆固醇氧化衍生物多达上百种。具有代表性质的胆固醇氧化衍生物主要有7-酮基胆固醇、7-酮基胆甾醇-9-羧基壬酸酯、25-羟基胆固醇、7β-羟基胆固醇、3β,5α,6β.三羟基胆固烷等化合物,这些衍生物广泛存在于胆固醇膳食、高胆固醇血症的血浆、动脉组织、人动脉粥样硬化斑块、斑块内的泡沫细胞、以及氧化型低密度脂蛋白中。大量实验表明胆固醇氧化衍生物对动脉粥样硬化形成有关因素(炎症、氧化应激、凋亡)具有促进作用。提示,胆固醇氧化衍生物在动脉粥样硬化的发生和发展中具有重要的作用。  相似文献   

11.
对PPAR-γ的激动剂及其在动脉粥样硬化中对血管细胞的影响等方面进行综述。过氧化物酶体增殖物激活受体-γ(peroxisome proliferator—activatedreceptor-γ,PPAR-γ)几乎对参与动脉粥样硬化的所有血管细胞均有影响,在调节动脉粥样硬化的发生中起重要的作用。PPAR-γ与特异性激动剂结合后,调节靶基因的转录活性,抑制血管细胞的增殖与迁移,降低炎症反应,阻止动脉粥样硬化的发生。  相似文献   

12.
分别用浓度0.02、0.04、0.06、0.08和0.10g/L的蓖麻毒蛋白对泥鳅进行急性毒性试验,在染毒处理第1、3、7、11d时将泥鳅断尾制血涂片,观察红细胞的凋亡情况.结果表明:蓖麻毒蛋白对泥鳅红细胞的凋亡具有明显的浓度和时间依赖性;染毒初期,泥鳅红细胞的凋亡率随蓖麻毒蛋白浓度的升高而不断增加;随染毒处理时间的延长,凋亡率曲线达峰值,随后凋亡率曲线不断降低,整个凋亡率曲线呈抛物线形.结论:蓖麻毒蛋白能诱导泥鳅红细胞凋亡.  相似文献   

13.
目的:究动脉粥样硬化对SMC凋亡及凋亡相关基因表达的影响,探讨凋亡的分子机制及晚期AS斑块破裂之原因。方法:采用高维生素D3 高脂肪高胆固醇饲料喂养法建立大鼠AS的模型;运用DNA琼脂糖凝胶电泳法鉴定基因组DNA的断裂情况;使用Northern Blot检测P53、c-myc及bcl-2基因的表达活性。结果:a.AS斑块中SMC的DNA片断在电泳中呈特征性梯状分布;b.AS斑块中P53及C-myc基因转录明显增强;c.AS斑块中SMC的bcl-2mRNA含量显著下降。提示1.AS斑块中存在凋亡的SMC,P53及C-myc表达的增强和bcl-2的表达下调介导了这一过程;2.SMC的凋亡可能是晚期AS斑块玻裂的重要原因。  相似文献   

14.
Background:The adhesion of monocytes to the endothelium following accumulation oflow-density lipoprotein(LDL) in subendothelial spaces is an important step in the development of intimal hyperplasia in arterially implanted vein grafts and atherosclerosis in both animals and humans.However.it iS not well known how serum factors affect the adhesion of monocytes.Methods:We have studied the efrect of fetal calf serum(FCS).which we considered a source of LDL.on the adhesion of monocytes to endothelial cells(Ecs)by using human monocytic THP-1 cells and both a monolayer of cultured bovine aortic endothelial cells(EC monoculture)and a co-culture with bovine aortic smooth muscle cells(EC-SMC co-culture).Results:It was found that the addition of FCS to the medium greatly affected the adhesion of THP-1 cells,and the higher the concentration of FCS in the medium,the greater the adhesion of THP-1 cells to endothelial cells.Adhesion of THP-1 cells to an EC-SMC co-culture Was approximately twofold greater than that to an EC monoculture,and after adhering to endothelial cells,many THP-1 cells transmigrated into the layer of smooth muscle cells.Conclusion:The results suggest that the elevation of the LDL(cholesterol)level in blood provides a favorable condition for the development of intimal hyperplasia and atherosclerosis by promoting the adhesion of monocytcs to the endothelium and their subsequent migration into subendothelial spaces.  相似文献   

15.
[目的]研究三氧化二砷对人红白血病细胞株K562凋亡作用及凋亡推测办法.[方法]姬姆萨染色,胎盘兰排染法,双苯并咪唑,碘化丙啶排斥法等.[结果]As2O3诱导12h,K562细胞开始出现凋亡.凋亡细胞随药物浓度的增加和作用时间的延长而增加.各种凋亡推测方法利弊存在差异.[结论]建议使用较有效的Hoechst33342法检测凋亡.  相似文献   

16.
[目的]研究三氧化二砷对K562细胞凋亡的诱导.[方法]采用人红白血病细胞株K562细胞常规培养,给不同浓度的三氧化二砷,在不同的时间收获细胞,用台盼蓝排染法,DNA荧光染料Hoechst33342荧光染色法,及碘化丙啶(PI)与Hoechst33342共染计数坏死细胞的PI阳性率等方法,检测其对K562细胞的影响.[结果]三氧化二砷能够诱导K562细胞凋亡.并且呈现浓度依赖性和时间依赖性.[结论]三氧化二砷主要以诱导肿瘤细胞凋亡而表现其毒性作用.  相似文献   

17.
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   

18.
This paper aims to investigate the effects of artesunate (ART) on growth and apoptosis in human osteosarcoma HOS cell line in vitro and in vivo and to explore the possible underlying mechanisms. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The induction of apoptosis was detected by light and transmission electron microscopy and flow cytometry. Western blot analysis was used to investigate the related mechanisms. Nude mice were further employed to investigate the antitumour activity of ART in vivo. MTT assay results demonstrated that ART selectively inhibits the growth of HOS cells in a dose- and time-dependent manner. Based on the findings of light and transmission electron microscopy, Hoechst 33258 staining, and fluorescein isothiocyanate (FITC)-annexin V staining, the cytotoxicity of ART in HOS cells occurs through apoptosis. With ART treatment, cytosolic cytochrome c was increased, Bax expression was gradually upregulated, Bcl-2 expression was downregulated, and caspase-9 and caspase-3 were activated. Thus, the intrinsic apoptotic pathway may be involved in ART-induced apoptosis. Cell cycle analysis by flow cytometry indicated that ART may induce cell cycle arrest at G2/M phase. In nude mice bearing HOS xenograft tumours, ART inhibited tumour growth and regulated the expressions of cleaved caspase-3 and survivin, in agreement with in vitro observations. ART has a selective antitumour activity against human osteosarcoma HOS cells, which may be related to its effects on induction of apoptosis via the intrinsic pathway. The results suggest that ART is a promising candidate for the treatment of osteosarcoma.  相似文献   

19.
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   

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