共查询到19条相似文献，搜索用时 296 毫秒
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目的:研究淫羊藿多糖对卵泡细胞凋亡的作用及机理。方法:对4周龄健康雌性小鼠连续灌服不同剂量淫羊藿多糖7 d,并采集各组小鼠卵巢卵泡细胞,检测卵泡细胞凋亡情况,RT-PCR检测凋亡相关基因Bcl-2/Bax表达水平;同时完整分离心脏、肝脏、脾脏、肺脏和肾脏,称重并计算各组内脏指数。结果:8、6 mg组和生理盐水对照组的卵泡细胞总凋亡率分别为10.89%、8.75%和11.74%;RT-PCR技术测定Bcl-2和Bax凋亡相关基因的表达发现,抑制凋亡基因Bcl-2 mRNA的表达显著升高。结论:淫羊藿多糖可有效抑制小鼠卵巢卵泡细胞凋亡,这一作用主要与调节细胞凋亡的Bcl-2/Bax基因表达有关。 相似文献
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近年来 ,细胞凋亡已成为生物医学研究领域中的一个热点 ,细胞凋亡过程复杂 ,有许多因子参与其中 ,Bcl- 2蛋白家族是细胞凋亡研究中最受关注的蛋白类群 ,它是细胞凋亡信号转导的主要调节物 ,在细胞凋亡过程中发挥重要的作用。B细胞淋巴瘤 /白血病 - 2 (B -celllymphoma/leukemia- 2 ,Bcl- 2 )基因是第一个被发现的能抑制多种细胞凋亡的原癌基因 ,它是Bcl- 2蛋白家族基因的原型。Bcl- 2基因最初是从人的滤泡性B细胞淋巴瘤中分离出来的 ,通常它定位于人的第 18号染色体。Bcl - 2蛋白由 2 39个氨基酸组成 ,分子量为 2 5～2 6KD。大多数Bcl-… 相似文献
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目的:评估茶多酚对人乳腺癌细胞MCF-7凋亡的影响,并探讨了其作用机制。创新点:全面考察了茶多酚对抗乳腺癌的分子机制,为茶多酚作为抗肿瘤辅助药物提供理论依据。方法:首先选取不同组织来源的五种人肿瘤细胞(人肝癌细胞Hep G2、人肺癌细胞A549、人前列腺癌细胞PC3、人宫颈癌细胞Hela、人乳腺癌细胞MCF-7)作为体外模型,以MTT法检测茶多酚对其增殖抑制作用。然后,选用最敏感细胞MCF-7为研究对象,采用流式细胞术检测茶多酚对细胞周期分布的影响,用Hoechst 3328染色法观察茶多酚对细胞核形态的影响,用JC-1染色法观察茶多酚对细胞线粒体跨膜电位的影响,用双氯荧光素(DCFH-DA)染色法观察茶多酚对细胞活性氧(ROS)水平的影响,用凝胶电泳DNA片段测定法(DNA ladder)观察茶多酚处理后细胞DNA断裂情况,用蛋白质印迹法(Western blot)检测茶多酚对细胞凋亡关键蛋白caspase-3和caspase-9表达的影响,全面探讨了茶多酚体外抗肿瘤机制。结论:实验结果显示,茶多酚能够通过诱导细胞周期阻滞和线粒体凋亡抑制MCF-7细胞增殖。茶多酚诱导线粒体凋亡的途径是使线粒体跨膜电位下降,促使MCF-7细胞内ROS生成,促使细胞DNA断裂和促进细胞内caspase-3和caspase-9的活化。 相似文献
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王羽 《湖北广播电视大学学报》2010,30(12):154-155
凋亡是一种不同于坏死且受基因控制的主动性细胞自我消亡过程,亦是许多抗癌药物作用的主要机理之一。Bcl-2是一种凋亡负控制的重要基因,其蛋白产物能抑制细胞的凋亡或程序性细胞死亡过程。我们构建了反义bcl-2逆转录病毒表达载体导入多发性骨髓瘤细胞株来调节Bcl-2基因表达,从而诱导细胞凋亡或增加细胞对凋亡诱导剂的敏感性,来探讨与多发些骨髓瘤的关系。 相似文献
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论文通过文献资料法、逻辑分析法等对骨髓间充质干细胞作用于心肌细胞凋亡应用,以及心肌细胞凋亡与Bcl-2和Bax蛋白表达的关系进行研究,旨在探讨骨髓间充质干细胞调控Bcl-2、Bax基因蛋白表达的方式对心肌细胞凋亡的作用机制。研究发现,心肌细胞凋亡与Bcl-2、Bax基因蛋白的表达存在高度相关性,通过调控Bcl-2、Bax的基因表达能够在一定程度上防止心肌细胞凋亡的发生与发展,而骨髓间充质干细胞则可以通过自身诱导分化的特性有效的调控Bcl-2和Bax蛋白的表达,使损伤后的心肌功能得到改善。 相似文献
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益肾强心合剂对慢性心衰大鼠心肌细胞凋亡的影响 总被引：1，自引：1，他引：0
目的:观察益肾强心合剂对慢性心衰大鼠心肌细胞凋亡的影响.方法:以皮下大量注射异丙肾上腺素(ISO)的方法制备慢性心衰大鼠模型.造模成功后随机分为模型对照组、卡托普利组及益肾强心合剂大、小剂量组,另设正常对照组,给药四周.TUNEL法检测心肌细胞凋亡指数,免疫组化方法检测心肌细胞Bax、Bcl-2蛋白表达,计算Bcl-2/Bax比值.结果:模型对照组心肌细胞凋亡指数、Bax促凋亡蛋白表达明显增加,Bcl-2抑凋亡蛋白表达减少、Bcl-2/Bax的比值明显降低,与正常对照组比较有显著性差异(P<0.05);益肾强心合剂大、小剂量组凋亡指数、Bax蛋白显著降低,Bcl-2蛋白明显增加、Bcl-2/Bax比值明显升高,与模型对照组比较有显著性差异(P<0.05).结论:益肾强心合剂对慢性心衰心肌细胞凋亡有良好的抑制作用,是防治慢性心衰(CHF)的有效药物. 相似文献
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《赤峰学院学报(自然科学版)》2016,(16)
目的:探讨黄芪注射液对大鼠肝缺血再灌注损伤的保护作用,进一步讨论其对细胞凋亡的作用机制.方法:72只健康雄性SD大鼠,随机分为假手术组、缺血再灌注组、缺血预处理组和黄芪注射液预处理组,每组按再灌注(1h,6h,24h)三个时间点分3个亚组.建立动物模型;测定组织中Bcl-2、Bax蛋白表达情况及肝组织凋亡指数(AI);通过透射电镜观察大鼠肝细胞的形态变化.结果:与Sham组相比,IR、IP、A组肝组织中Bcl-2、Bax蛋白表达以及AI均增加(P0.05);与IR组比,IP、A组肝组织Bax蛋白的表达及AI减少,而Bcl-2蛋白表达增加(P0.05);与IP组比,A组肝组织Bax蛋白的表达及AI减少,而Bcl-2蛋白的表达增加(P0.05).通过透射电镜下对肝细胞学观察,可见Sham组肝细胞形态基本正常,IR组损伤最重,IP及A组肝细胞损伤程度较IR组轻,A组更轻.结论:IP及黄芪注射液都可通过抑制Bax蛋白的表达,上调Bcl-2蛋白的表达,来减轻肝细胞凋亡,相比之下后者效果要更好. 相似文献
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目的:观察姜黄素对人乳腺癌MCF-7细胞(简称MCF-7细胞)凋亡的诱导作用.方法:不同浓度姜黄素(0.048,0.056,0.064,0.072,0.080μmol/L)作用于MCF-7细胞24h,采用CCK-8法检测其对MCF-7细胞的生长抑制作用;琼脂糖凝胶电泳检测细胞凋亡结果.结果:经上述不同浓度姜黄素诱导24h后,MCF-7细胞生长抑制率分别为17%、28%、48%、50%及55%;琼脂糖凝胶电泳显示出DNA梯形条带.结论:姜黄素对体外培养MCF-7细胞的增殖有明显的抑制作用并可诱导其细胞凋亡. 相似文献
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通过游泳方法建立运动模型,观察不同运动负荷状态下大鼠肾脏组织病理变化.一般负荷运动组肾小管排列略紊乱,肾小球轻度肿大,超负荷运动组肾小管排列紊乱,肾小囊变小甚至消失,而对照组无变化.应用免疫组化法检测Bcl-2蛋白在不同负荷运动组的表达情况.超负荷运动组Bcl-2蛋白的表达比一般负荷组及对照组有显著性的降低(P＜0.05),一般负荷运动组Bcl-2蛋白表达与对照组相比没有显著性差异.应用末端脱氧核苷转移酶介导的缺口标记法检测大鼠肾脏组织细胞凋亡情况.一般负荷组细胞凋亡比对照组有显著性增加(P＜0.05),超负荷组与一般负荷组相比有显著性增加(P＜0.05),细胞凋亡的可能机制是:超负荷的运动刺激导致线粒体膜受到损伤,促使其释放了促凋亡因子,诱导了细胞的凋亡.研究结果表明:过度训练对肾脏组织结构造成一定损伤,使肾脏细胞凋亡增加,这或许是过度训练导致运动疲劳的原因之一. 相似文献
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《洛阳师范学院学报》2021,(2)
在白杨素的7-位羟基上进行修饰,对得到的C~7-位白杨素衍生物进行生物活性研究.通过MTT法检测其对人子宫颈癌细胞(HeLa)、人乳腺癌细胞(MCF-7)、人胃癌细胞(A549)等细胞增殖的抑制作用,通过AV-PI双染法流式细胞仪检测细胞凋亡状况.结果显示,C~7-位白杨素衍生物对HeLa、 MCF-7、 A549细胞都有一定的抗增殖作用,其中对HeLa细胞的抗增值效果最好,IC_(50)值为20.62μmol/L;当药物浓度为20μmol/L时,细胞凋亡率达到22.32%,说明C~7-位白杨素衍生物具有良好的抗癌活性. 相似文献
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In order to study the molecular mechanisms of green tea polyphenols (GTPs) in treatment or prevention of breast cancer, the cytotoxic effects of GTPs on five human cell lines (MCF-7, A549, Hela, PC3, and HepG2 cells) were determined and the antitumor mechanisms of GTPs in MCF-7 cells were analyzed. The results showed that GTPs exhibited a broad spectrum of inhibition against the detected cancer cell lines, particularly the MCF-7 cells. Studies on the mechanisms revealed that the main modes of cell death induced by GTPs were cell cycle arrest and mitochondrialmediated apoptosis. Flow cytometric analysis showed that GTPs mediated cell cycle arrest at both G1/M and G2/M transitions. GTP dose dependently led to apoptosis of MCF-7 cells via the mitochondrial pathways, as evidenced by induction of chromatin condensation, reduction of mitochondrial membrane potential (ΔΨm), improvement in the generation of reactive oxygen species (ROS), induction of DNA fragmentation, and activations of caspase-3 and caspase-9 in the present paper. 相似文献
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Bcl-2家族是研究的最早与凋亡相关的因子,发挥抗凋亡或促凋亡的作用,是线粒体凋亡通路中最主要的调节因子。近年来对于Bcl-2家族的研究取得了很大的进展,个别Bcl-2家族成员不仅具有凋亡调节作用,与细胞增殖也密切相关,从而将细胞周期与细胞凋亡偶连。本文较全面地综述了Bcl-2家族中Bcl-2、Bax及Bid三个成员与细胞周期关系的研究新进展。 相似文献
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川芎嗪对人乳腺癌MCF-7/ADM细胞多药耐药性的逆转及P-糖蛋白表达的影响 总被引：2，自引：0，他引：2
[目的]探讨川芎嗪(TMP)对人乳腺癌MCF-7/ADM细胞的耐药逆转及其对该细胞P-糖蛋白(P-gp)表达的影响.[方法]MTT法测定细胞的药敏性和抗药性逆转,流式细胞术检测耐药细胞P-糖蛋白的表达.[结果]非细胞毒性剂量(320μg/m l)和低毒剂量(1 250μg/m l)的川芎嗪均能显著降低MCF-7/ADM细胞的IC50(P<0.01),逆转倍数分别为2.14和2.80倍;并使该细胞P-gp的表达率由(90.60±0.40)%分别降低至(69.10±1.65)%和(60.30±1.25)%.[结论]川芎嗪可部分逆转人乳腺癌MCF-7/ADM细胞对阿霉素的耐药性,其逆转机制与抑制该细胞P-gp的表达有关. 相似文献
15.
目的探讨银杏叶总黄酮对体外培养的人肝癌HepG2细胞凋亡的促进作用及其分子机理。方法采用TUNEL法检测银杏叶总黄酮对HepG2细胞凋亡的影响,提取Bcl-2基因的mRNA,以RT-PCR法研究银杏叶总黄酮对Bcl-2基因表达的影响。结果银杏叶总黄酮使人HepG2细胞凋亡指数增加（P〈0．01）,且呈剂量依赖效应;Bcl-2基因mRNA水平随银杏叶总黄酮浓度升高而降低。结论银杏叶总黄酮可促进人HepG2细胞的凋亡过程,并使Bcl-2基因mRNA水平降低,从而起到抗肿瘤的治疗作用。 相似文献
16.
Feng Gao Xin-yang Hu Xiao-jie Xie Qi-yuan Xu Ya-ping Wang Xian-bao Liu Mei-xiang Xiang Yong Sun Jian-an Wang 《Journal of Zhejiang University. Science. B》2010,11(8):608-617
Mesenchymal stem cell(MSC)transplantation has shown a therapeutic potential to repair the ischemic and infracted myocardium,but the effects are limited by the apoptosis and loss of donor cells in host cardiac microenvironment.The aim of this study is to explore the cytoprotection of heat shock protein 90(Hsp90)against hypoxia and serum deprivation-induced apoptosis and the possible mechanisms in rat MSCs.Cell viability was determined by3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assay.Apoptosis was assessed by Hoechst 33258nuclear staining and flow cytometric analysis with annexin V/PI staining.The gene expression of Toll-like receptor-4(TLR-4)and V-erb-b2 erythroblastic leukemia viral oncogene homolog 2(ErbB2)was detected by real-time polymerase chain reaction(PCR).The protein levels of cleaved caspase-3,Bcl-2,Bcl-xL,Bax,total-ERK,phospho-ERK,totaI-Akt,phospho-Akt,and Hsp90 were detected by Western blot.The production of nitric oxide was measured by spectrophotometric assay.Hsp90 improves MSC viability and protects MSCs against apoptosis induced by serum deprivation and hypoxia.The protective role of Hsp90 not only elevates Bcl-2/Bax and Bcl-xL/Bax expression and attenuates cleaved caspase-3 expression via down-regulating membrane TLR-4 and ErbB2 receptors and then activating their downstream PI3K/Akt and ERK1/2 pathways,but also enhances the paracrine effect of MSCs.These findings demonstrated a novel and effective treatment strategy against MSC apoptosis in cell transplantation. 相似文献
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DNA-damage response network at the crossroads of cell-cycle checkpoints,cellular senescence and apoptosis 总被引：2，自引：0，他引：2
Schmitt E Paquet C Beauchemin M Bertrand R 《Journal of Zhejiang University. Science. B》2007,8(6):377-397
Tissue homeostasis requires a carefully-orchestrated balance between cell proliferation, cellular senescence and cell death. Cells proliferate through a cell cycle that is tightly regulated by cyclin-dependent kinase activities. Cellular senescence is a safeguard program limiting the proliferative competence of cells in living organisms. Apoptosis eliminates unwanted cells by the coordinated activity of gene products that regulate and effect cell death. The intimate link between the cell cycle, cellular senescence, apoptosis regulation, cancer development and tumor responses to cancer treatment has become eminently apparent. Extensive research on tumor suppressor genes, oncogenes, the cell cycle and apoptosis regulatory genes has revealed how the DNA damage-sensing and -signaling pathways, referred to as the DNA-damage response network, are tied to cell proliferation, cell-cycle arrest, cellular senescence and apoptosis. DNA-damage responses are complex, involving ＂sensor＂ proteins that sense the damage, and transmit signals to ＂transducer＂ proteins, which, in turn, convey the signals to numerous ＂effector＂ proteins implicated in specific cellular pathways, including DNA repair mechanisms, cell-cycle checkpoints, cellular senescence and apoptosis. The Bcl-2 family of proteins stands among ＂the mos＂t crucial regula＂tors of apop＂tosis and performs vi＂tal func＂tions in deciding whether a cell will live or die after cancer chemotherapy and irradiation. In addition, several studies have now revealed that members of the Bcl-2 family also interface with the cell cycle, DNA repair/recombination and cellular senescence, effects that are generally distinct from their function in apoptosis. In this review, we report progress in understanding the molecular networks that regulate cell-cycle checkpoints, cellular senescence and apoptosis after DNA damage, and discuss the influence of some Bcl-2 family members on cell-cycle checkpoint regulation. 相似文献
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Wang Guan Hao Mingyue Liu Qiong Jiang Yanlong Huang Haibin Yang Guilian Wang Chunfeng 《Journal of Zhejiang University. Science. B》2021,22(5):348-365
This study probed the protective effect of recombinant Lactobacillus plantarum against hydrogen peroxide(H_2O_2)-induced oxidative stress in human umbilical vein endothelial cells(HUVECs). We constructed a new functional L. plantarum(NC8-p SIP409-alr-angiotensin-converting enzyme inhibitory peptide(ACEIP)) with a double-gene-labeled non-resistant screen as an expression vector. A 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2 H-tetrazolium bromide(MTT) colorimetric assay was carried out to determine the cell viability of HUVEC cells following pretreatment with NC8-p SIP409-alr-ACEIP. Flow cytometry(FCM) was used to determine the apoptosis rate of HUVEC cells. Cysteinyl aspartate specific proteinase(caspase)-3/8/9 activity was also assayed and western blotting was used to determine protein expression of B-cell lymphoma 2(Bcl-2), Bcl-2-associated X protein(Bax), inducible nitric oxide synthase(i NOS), nicotinamide adenine dinucleotide phosphate oxidase 2(gp91 phox), angiotensin II(Ang II), and angiotensin-converting enzyme 2(ACE2), as well as corresponding indicators of oxidative stress, such as reactive oxygen species(ROS), mitochondrial membrane potential(MMP), malondialdehyde(MDA),and superoxide dismutase(SOD). NC8-p SIP409-alr-ACEIP attenuated H_2O_2-induced cell death, as determined by the MTT assay. NC8-p SIP409-alr-ACEIP reduced apoptosis of HUVEC cells by FCM. In addition, compared to the positive control, the oxidative stress index of the H_2O_2-induced HUVEC(Hy-HUVEC), which was pretreated by NC8-p SIP409-alr-ACEIP, i NOS,gp91 phox, MDA, and ROS, was decreased obviously; SOD expression level was increased; caspase-3 or-9 was decreased, but caspase-8 did not change; Bcl-2/Bax ratio was increased; permeability changes of mitochondria were inhibited; and loss of transmembrane potential was prevented. Expression of the hypertension-related protein(Ang II protein) in HUVEC cells protected by NC8-p SIP409-alr-ACEIP decreased and expression of ACE2 protein increased. These plantarum results suggested that NC8-p SIP409-alr-ACEIP protects against H_2O_2-induced injury in HUVEC cells. The mechanism for this effect is related to enhancement of antioxidant capacity and apoptosis. 相似文献