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人参皂苷Rg3对大鼠血管平滑肌细胞凋亡及凋亡相关基因表达的影响 认领
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作者 仇治梅 陈文明 +1 位作者 王艳 石蓓 《遵义医科大学学报》 2020年第4期419-424,共6页
目的研究人参皂苷Rg3(Ginsenoside Rg3,GSRg3)对大鼠血管平滑肌细胞(Vascular smooth muscle cells,VSMCs)凋亡的影响及可能的作用机制。方法采用组织块贴壁法培养大鼠VSMCs,免疫荧光法检测VSMCs中平滑肌α-肌动蛋白(Smooth muscle alph... 目的研究人参皂苷Rg3(Ginsenoside Rg3,GSRg3)对大鼠血管平滑肌细胞(Vascular smooth muscle cells,VSMCs)凋亡的影响及可能的作用机制。方法采用组织块贴壁法培养大鼠VSMCs,免疫荧光法检测VSMCs中平滑肌α-肌动蛋白(Smooth muscle alpha actin,SMα-actin);MTT法检测不同浓度GSRg3(25、50、100μg/mL)和不同时间(24、48 h)刺激下对VSMCs的增殖效应;Annexin V-FITC/PI双标记流式细胞术检测GSRg3处理VSMCs凋亡情况;Western blot检测Bax、Bcl-2、cleaved caspase 3、cleaved caspase 9蛋白的表达水平。结果MTT检测结果显示,与对照组相比,不同浓度GSRg3组VSMCs增殖活性下降,且呈时间和剂量依赖性(P<0.05);Annexin V-FITC/PI双标记流式细胞术检测结果显示,与对照组相比,不同浓度GSRg3作用于VSMCs 48 h后凋亡率明显增加(P<0.05);Western blot结果显示,与对照组相比,GSRg3能够下调抗凋亡蛋白Bcl-2的表达,上调促凋亡蛋白Bax、cleaved caspase 3和cleaved caspase 9的表达,并呈浓度依赖性(P<0.05)。结论GSRg3通过促进Bax、cleaved caspase 3和cleave caspase 9的表达,抑制Bcl-2的表达,从而诱导VSMCs凋亡。 展开更多
关键词 人参皂苷RG3 血管平滑肌细胞 细胞凋亡 凋亡相关基因
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miR-144通过靶向TIGAR调控胃癌细胞增殖与凋亡及自噬的分子机制 认领
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作者 谭业儒 伍小平 李跃华 《中国临床药理学杂志》 CAS CSCD 北大核心 2020年第1期57-60,共4页
目的研究miR-144对胃癌细胞增殖、凋亡和自噬的影响和机制。方法将miR-144 mimics、mimics control分别转染胃癌细胞,依次标记为mimics-NC组、miR-144 mimics组。将miR-144 mimics分别与pcDNA3.1、pcDNA3.1-TIGAR共转染至胃癌细胞,依次... 目的研究miR-144对胃癌细胞增殖、凋亡和自噬的影响和机制。方法将miR-144 mimics、mimics control分别转染胃癌细胞,依次标记为mimics-NC组、miR-144 mimics组。将miR-144 mimics分别与pcDNA3.1、pcDNA3.1-TIGAR共转染至胃癌细胞,依次标记为miR-144 mimics+NC组、miR-144 mimics+TIGAR组。正常培养的胃癌细胞标记为Control组。以噻唑蓝法检测细胞增殖,以流式细胞术测定细胞凋亡,以Western blot检测凋亡蛋白caspase-3和自噬蛋白Beclin1、LC3Ⅱ/Ⅰ表达变化,以生物信息学软件预测miR-144的靶基因可能为TIGAR,利用荧光素酶报告系统鉴定靶向关系。结果 mimics-NC组和miR-144 mimics组的细胞增殖能力分别为0.36±0.05,0.20±0.02,细胞凋亡率分别为3.05±0.34,13.84±1.47,caspase-3表达水平分别为0.22±0.04,0.43±0.05, Beclin1分别为0.38±0.06,0.73±0.07,LC3Ⅱ分别为0.19±0.03,0.39±0.05,差异均有统计学意义(均P<0.05)。miR-144 mimics+NC组和miR-144 mimics+TIGAR组的细胞增殖能力分别为0.21±0.04,0.32±0.03,细胞凋亡率分别为12.04±1.25,5.98±0.73,caspase-3表达水平分别为0.40±0.03,0.24±0.05,Beclin1分别为0.60±0.05,0.46±0.06,LC3Ⅱ分别为0.34±0.06,0.20±0.03,差异均有统计学意义(均P<0.05)。结论 miR-144靶向抑制TIGAR表达降低胃癌细胞增殖能力,并诱导胃癌细胞凋亡和自噬。 展开更多
关键词 胃癌细胞 自噬 凋亡 TP53诱导的糖酵解和凋亡调节因子
Piperlongumine inhibits cell growth and enhances TRAIL-induced apoptosis in prostate cancer cells 认领
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作者 Gorkem Kismali Ahmet Ceylan +6 位作者 Ogunc Meral Merve Alpay Funda Kosova Dilek Ulker Cakir Begum Yurdakok-Dikmen Neslihan Tascene Tevhide Sel 《亚太热带生物医学杂志:英文版》 SCIE CAS 2020年第5期216-223,共8页
Objective: To investigate whether piperlongumine can sensitize prostate cancer cells to tumor necrosis factor-related apoptosisinducing ligand(TRAIL) and trigger apoptosis in prostate cells. Methods: Human prostate ca... Objective: To investigate whether piperlongumine can sensitize prostate cancer cells to tumor necrosis factor-related apoptosisinducing ligand(TRAIL) and trigger apoptosis in prostate cells. Methods: Human prostate cancer cell lines PC3, LNCa P, and VCa P were cultured with piperlongumine and TRAIL. Then, cell proliferation, migration, caspase activation, apoptotic protein expressions, and death receptor expressions were measured.Results: Piperlongumine inhibited cell proliferation at low doses(<10 μM) alone and in combination with TRAIL(25 ng/m L), induced apoptosis, and suppressed cyclooxygenase activation. Additionally, piperlongumine induced expression of death receptors which potentiated TRAIL-induced apoptosis in cancer cells but did not affect decoy receptors. Piperlongumine also downregulated tumor cell-survival pathways, inhibited colony formation and migration of cancer cells alone or in combination with TRAIL. The combination of piperlongumine with TRAIL was found to be synergistic. Conclusions: Our findings indicate that piperlongumine can sensitize cancer cells to TRAIL through the upregulation of death receptors and can trigger apoptosis with the downregulation of antiapoptotic proteins. 展开更多
关键词 Piperlongumine PROSTATE cancer APOPTOSIS TUMOR NECROSIS factor-related apoptosis-inducing LIGAND
Cell Fleeing from Death Phenomenon 认领
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作者 Mahmoud Saad Mohamed El-Khodary 《细胞生物学(英文)》 2020年第1期1-13,共13页
Cell fleeing from death phenomenon occurs as either complete or incomplete;the phenomenon is incomplete fleeing from death when cell blocks intrinsic death program only. But, it becomes complete fleeing from death if ... Cell fleeing from death phenomenon occurs as either complete or incomplete;the phenomenon is incomplete fleeing from death when cell blocks intrinsic death program only. But, it becomes complete fleeing from death if the cell successfully blocks the pathway of intrinsic and extrinsic programs of cell death. This phenomenon is induced by the formation of hydrogen peroxide which activates nuclear factor kappa B. The nuclear factor-kappa B stimulates the expression of several genes, to produces 6 factors (BcL-2, Muc-1, MMPs, DcR3, Muc-4, muc-16, and TNF-α). Such factors act as blockers of the pathway of intrinsic and extrinsic programs of cell death. These blockers convert normal cell to a cancer cell. If these blockers are removed, the death programs of cancer cells will run again and cancer will disappear. 展开更多
关键词 Phenomenon APOPTOSIS CANCER
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DR5、FADD在子宫肌瘤组织中的表达水平及意义 认领
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作者 唐亮 王敏 +2 位作者 张利军 王梅 肖燕 《国际妇产科学杂志》 CAS 2020年第1期37-40,I0001共5页
目的:探讨死亡受体5(DR5)、凋亡促进蛋白(FADD)在子宫肌瘤组织中的表达情况及临床意义。方法:选取2017年3月-2018年5月在本院进行子宫肌瘤切除术的72例患者作为研究对象,将手术切除的子宫肌瘤组织为肌瘤组织组,距离肿瘤边缘5 cm以外的... 目的:探讨死亡受体5(DR5)、凋亡促进蛋白(FADD)在子宫肌瘤组织中的表达情况及临床意义。方法:选取2017年3月-2018年5月在本院进行子宫肌瘤切除术的72例患者作为研究对象,将手术切除的子宫肌瘤组织为肌瘤组织组,距离肿瘤边缘5 cm以外的瘤旁组织为瘤旁组织组。采用实时荧光定量聚合酶链反应(qRT-PCR)检测DR5和FADD的表达量;免疫组织化学法检测DR5和FADD的表达情况;用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记测定法(TUNEL)统计细胞凋亡的情况,并分析DR5和FADD与细胞凋亡及两者的相关性。结果:肌瘤组织组DR5 m RNA、蛋白阳性表达率均高于瘤旁组织组(P<0.05),FADD mRNA、蛋白阳性表达率均低于瘤旁组织组(P<0.05);肌瘤组织组凋亡指数(AI)低于瘤旁组织组,增殖指数(PI)高于瘤旁组织组(P<0.05);在子宫肌瘤组织中,DR5的表达与AI呈负相关(P<0.05),与PI呈正相关(P<0.05),FADD的表达与AI呈正相关(P<0.05),与PI呈负相关(P<0.05);DR5与FADD呈负相关(P<0.05)。结论:在子宫肌瘤组织中,DR5高表达,FADD低表达,且两者均与AI、PI相关性明显,可能共同参与子宫肌瘤的发生发展。 展开更多
关键词 平滑肌瘤 受体 肿瘤坏死因子 细胞凋亡 凋亡调节蛋白质类 子宫肌瘤切除术
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Anti-proliferation and apoptosis-inducing effects of sodium aescinate on retinoblastoma Y79 cells 认领
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作者 Lei Li Bing Xu +6 位作者 Cai-Rui Li Miao-Miao Zhang Sheng-Jun Wu Wen-Jun Dang Jing-Chen Liu Shu-Guang Sun Wei Zhao 《国际眼科杂志:英文版》 SCIE CAS 2020年第10期1546-1553,共8页
AIM:To investigate the anti-proliferation and apoptosisinducing effects of sodium aescinate(SA)on retinoblastoma Y79 cells and its mechanism.METHODS:Y79 cells were cultured at different drug concentrations for differe... AIM:To investigate the anti-proliferation and apoptosisinducing effects of sodium aescinate(SA)on retinoblastoma Y79 cells and its mechanism.METHODS:Y79 cells were cultured at different drug concentrations for different periods of time(24,48,and 72 h).The inhibitory effect of SA on proliferation of Y79 cells was detected by the cell counting kit-8(CCK-8)assay,and the morphology of Y79 cells in each group was observed under an inverted microscope.An IC50 of 48 h was selected for subsequent experiments.After pretreatment with SA for 24 and 48 h,cellular DNA distribution and apoptosis were detected by flow cytometry.Real-time qunatitative polymerase chain reaction(RT-qPCR)and Western blot were used to assess changes in related genes(CDK1,CyclinB1,Bax,Bcl-2,caspase-9,caspase-8,and caspase-3).RESULTS:SA inhibited proliferation and induced apoptosis of Y79 cells in a time-dependent and concentrationdependent manner.Following its intervention in the cell cycle pathway,SA can inhibit the expression of CDK1 and Cyclin B1 at the mRNA and protein levels,and block cells in the G2/M phase.In caspase-related apoptotic pathways,up-regulation of Bax and down-regulation of Bcl-2 caused caspase-9 to self-cleave and further activate caspase-3.What’s more,the caspase-8-mediated extrinsic apoptosis pathway was activated,and the activated caspase-8 was released into the cytoplasm to activate caspase-3,which as a member of the downstream apoptotic effect group,initiates a caspase-cascade reaction that induces cell apoptosis.CONCLUSION:SA inhibits the proliferation of Y79 cells by arresting the cell cycle at the G2/M phase,and induces apoptosis via the caspase-related apoptosis pathway,indicating that SA may have promising potential as a chemotherapeutic drug. 展开更多
关键词 sodium aescinate RETINOBLASTOMA intrinsic apoptosis pathway extrinsic apoptosis pathway cell cycle arrest
高压氧治疗对局灶性脑梗死大鼠的神经保护作用 认领
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作者 于秋红 李婕 +3 位作者 刘亚玲 王丛 任梓齐 薛连璧 《中国卒中杂志》 2020年第8期829-835,共7页
目的观察单次9 h高压氧(hyp erbaric oxygen,HBO)治疗对局灶性脑梗死大鼠凋亡诱导因子(apoptosis-inducing factor,AIF)、线粒体膜电位(mitochondrial membrane potential,MMPo)的影响,探讨HBO治疗的神经保护作用。方法108只SD大鼠制作... 目的观察单次9 h高压氧(hyp erbaric oxygen,HBO)治疗对局灶性脑梗死大鼠凋亡诱导因子(apoptosis-inducing factor,AIF)、线粒体膜电位(mitochondrial membrane potential,MMPo)的影响,探讨HBO治疗的神经保护作用。方法108只SD大鼠制作永久性大脑中动脉闭塞模型,随机分为对照组和HBO组,每组各54只。造模成功3 h后,HBO组实行HBO干预,压力0.2 MPa持续9 h,对照组呼吸常压空气。采用Garcia评分评估大鼠神经功能,比较两组造模后13 h、24 h和72 h神经功能改善情况,并在各时间点检测大鼠缺血半暗带脑组织凋亡细胞数、线粒体和细胞核AIF表达及MMPo水平。结果①神经功能评分:HBO组13 h(P<0.001)、24 h(P=0.04)神经功能评分改善比对照组更明显。②凋亡细胞数:HBO组13 h、24 h凋亡细胞数较对照组更少(均P<0.001)。③AIF在线粒体和细胞核的表达:13 h、24 h、72 h各时间点HBO组AIF在线粒体的表达均较对照组多(均P<0.001);各时间点HBO组AIF在细胞核的表达均较对照组少(均P<0.001)。④MMPo:各时间点HBO组MMPo均高于对照组(均P<0.001)。结论HBO治疗可改善大鼠神经功能,稳定MMPo,抑制AIF由线粒体向细胞核转移可能是其神经保护作用的机制之一。 展开更多
关键词 高压氧 脑梗死 凋亡 凋亡诱导因子 线粒体膜电位
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重楼皂苷D对人胰腺癌细胞增殖和凋亡的影响 认领
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作者 萧梅芳 《中国中药杂志》 CAS CSCD 北大核心 2020年第6期1418-1422,共5页
重楼皂苷D(polyphyllin D)是重楼中的一种甾体皂苷单体,具有抗菌、镇痛、镇静、抗肿瘤等多种药理作用,但在胰腺癌中少有报道。该研究通过检测凋亡相关指标,探讨polyphyllin D对人胰腺癌Panc-1细胞增殖和凋亡的影响及相关作用机制。采用C... 重楼皂苷D(polyphyllin D)是重楼中的一种甾体皂苷单体,具有抗菌、镇痛、镇静、抗肿瘤等多种药理作用,但在胰腺癌中少有报道。该研究通过检测凋亡相关指标,探讨polyphyllin D对人胰腺癌Panc-1细胞增殖和凋亡的影响及相关作用机制。采用CCK-8法检测不同浓度的(0,1,2,3,4,5μg·μL-1)polyphyllin D分别处理胰腺癌Panc-1细胞24,48,72 h后,观察对细胞增殖的影响。采用流式细胞术对细胞周期、细胞线粒体膜电位(mitochondrial membrane protential,MMP)进行检测,Annexin-V-FITC/PI双染法检测细胞凋亡情况,Western blot法检测细胞色素C (cytochrome C,Cyto C),Bax,Bcl-2,cleaved caspase-3,cleaved caspase-9的蛋白表达情况。结果表明,与对照组相比,polyphyllin D能够时间和浓度依赖性地抑制Panc-1细胞的增殖活性。流式细胞术检测显示polyphyllin D能浓度依赖性使细胞阻滞于S期和G2/M期,MMP明显降低,细胞凋亡率随polyphyllin D作用浓度增加而增加。Western blot结果显示,polyphyllin D能浓度依赖性地上调Bax,Cyto C,cleaved caspase-3和cleaved caspase-9的蛋白表达水平,下调Bcl-2的蛋白表达水平。以上研究结果提示,polyphyllin D能抑制胰腺癌Panc-1细胞的增殖,其机制可能与阻滞细胞的生长周期以及通过线粒体途径诱导细胞的凋亡相关。 展开更多
关键词 重楼皂苷D 人胰腺癌细胞 细胞周期 凋亡 线粒体
STAT1 and STAT2 Null Cells Are Resistant to RNA-Induced Apoptosis Due to Deficiency in Constitutive and Inducible Apoptosis-Regulating Genes 认领
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作者 Farag Bleiblo Paul Michael +4 位作者 Chilakamarti V. Ramana T. C. Tai Joseph E. Parrillo Anand Kumar Aseem Kumar 《美国分子生物学期刊(英文)》 2020年第3期165-187,共23页
Although much progress has been made in identifying the signaling pathways that mediate viral RNA-induced apoptosis and activation of interferon-stimulated genes, the role that bacterial RNA plays in regulating these ... Although much progress has been made in identifying the signaling pathways that mediate viral RNA-induced apoptosis and activation of interferon-stimulated genes, the role that bacterial RNA plays in regulating these responses has remained undetermined. Herein, we identified bacterial RNA as a novel inducer of the apoptotic cell death. Unlike the parental cells, STAT1 and STAT2 mutants display apoptotic defects which were reversed by restoring the expression of wild type proteins. While STAT1 mutants lacking tyrosine-701 or a functional SH2 domain were effective as the wild-type protein in restoring the apoptotic response, the mutant carrying a point mutation at serine-727 of STAT1 was resistant to bacterial RNA-induced apoptosis. We also determined that the lack of apoptosis in the STAT1 and STAT2 mutants was correlated with the constitutive and inducible activation of apoptosis regulating proteins. Furthermore, we show that bacterial RNA induces transcriptional activation of STAT1, STAT2, IRF1, and ISGF3, which was impaired in STAT1 or STAT2 mutants. These observations suggested that the participation of STATs in regulating the apoptotic response is independent of their downstream functions as cytokine-induced transcriptional activators. In addition to bacterial immunity, the results presented here may also have implications in cellular pathophysiology and RNA-based therapy. 展开更多
关键词 STAT1 STAT2 APOPTOSIS Bacterial RNA
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Isoflavone Attenuates the Nuclear Transcription Factor Kappa B (NF-<i>κ</i>B) Activation on MPP<sup>+</sup>-Induced Apoptosis of PC12 Cells 认领
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作者 Weidong Cheng Anqi Huang +5 位作者 Li Zhang Depeng Feng Xiaoqian Sun Hengyi Xu Qianru Sun Xueli Li 《行为与脑科学期刊(英文)》 2020年第5期191-199,共9页
Objective: To explore the underlying molecular mechanisms of cellular response to the challenge by 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis of PC12 cells, an in vitro cell model for Parkinson’s disease, a... Objective: To explore the underlying molecular mechanisms of cellular response to the challenge by 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis of PC12 cells, an in vitro cell model for Parkinson’s disease, and the effect of NF-κB activation on the protection of Parkinson’s disease by Isoflavone (I). Methods: PC12 cells were used to establish the cell model of Parkinson’s disease, and are divided into five groups: control group;MPP+ group;I (Isoflavone) + MPP+ group;I group;SN-50 + MPP+ group. The content of NF-κB in PC12 cells was determined by immunocytochemistry;The viability of PC12 cells after treated with cell-permeable NF-κB inhibitor SN-50 and cell viability were measured by MTT assay;the expression levels of NF-κB p65 in cytoplasm and nuclear fractions were evaluated by western blot analysis;the mRNA expression of NF-κB p65 was analyzed by in situ hybridization (ISH). Results: Compared with the control group, the protein of NF-κB p65 both in cytoplasm and in nuclei was significantly higher than in I + MPP+ and MPP+ groups;similarly, the mRNA expression level of NF-κB p65 gene was also significantly higher;moreover, the protein expression of NF-κB p65 was much lower in I group (P + group, the protein of NF-κB p65 was significantly lower in I + MPP+ group, the mRNA expression level of NF-κB p65 gene was also significantly lower, and the protein expression level of NF-κB p65 was much lower in I + MPP+ group (P + group (P > 0.05). Conclusion: NF-κB activation is essential to MPP+-induced apoptosis in PC12 cells;but Isoflavone can inhibit the cell damage to some extent to execute its protective function, which may be involved in nigral neurodegeneration in patients with Parkinson’s disease. 展开更多
关键词 ISOFLAVONE PC12 Cell MPP+ Apoptosis NF-κB p65 NUCLEAR Transcription Factor KAPPA B Parkinson’s Disease
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Role of apoptosis-inducing factor in perinatal hypoxic-ischemic brain injury 认领
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作者 Juan Rodriguez Tao Li +2 位作者 Yiran Xu Yanyan Sun Changlian Zhu 《中国神经再生研究:英文版》 SCIE CAS 2021年第2期205-213,共9页
Perinatal complications,such as asphyxia,can cause brain injuries that are often associated with subsequent neurological deficits,such as cerebral palsy or mental retardation.The mechanisms of perinatal brain injury a... Perinatal complications,such as asphyxia,can cause brain injuries that are often associated with subsequent neurological deficits,such as cerebral palsy or mental retardation.The mechanisms of perinatal brain injury are not fully understood,but mitochondria play a prominent role not only due to their central function in metabolism but also because many proteins with apoptosis-related functions are located in the mitochondrion.Among these proteins,apoptosis-inducing factor has already been shown to be an important factor involved in neuronal cell death upon hypoxia-ischemia,but a better understanding of the mechanisms behind these processes is required for the development of more effective treatments during the early stages of perinatal brain injury.In this review,we focus on the molecular mechanisms of hypoxic-ischemic encephalopathy,specifically on the importance of apoptosis-inducing factor.The relevance of apoptosis-inducing factor is based not only because it participates in the caspase-independent apoptotic pathway but also because it plays a crucial role in mitochondrial energetic functionality,especially with regard to the maintenance of electron transport during oxidative phosphorylation and in oxidative stress,acting as a free radical scavenger.We also discuss all the different apoptosis-inducing factor isoforms discovered,focusing especially on apoptosis-inducing factor 2,which is only expressed in the brain and the functions of which are starting now to be clarified.Finally,we summarized the interaction of apoptosis-inducing factor with several proteins that are crucial for both apoptosis-inducing factor functions(prosurvival and pro-apoptotic)and that are highly important in order to develop promising therapeutic targets for improving outcomes after perinatal brain injury. 展开更多
关键词 apoptosis apoptosis inducing factor ASPHYXIA cell death free radical HYPOXIA-ISCHEMIA mitochondria NEONATES oxidative stress
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核酸内切酶G在帕金森病大鼠脑组织中的表达及意义 认领
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作者 武林 任真奎 +4 位作者 吕菊 谢鹏 胡玉梅 吴昌学 禹文峰 《贵州医科大学学报》 CAS 2020年第4期387-391,407共6页
目的:探讨核酸内切酶G(Endo-G)介导的非Caspase依赖性细胞凋亡在帕金森病(PD)发生发展中的作用和分子机制。方法:30只SPF级雄性SD大鼠均分为PD模型组(PD组)和对照组(Ctrl组),PD组大鼠右侧纹状体注射6-羟多巴胺(6-OHDA)诱导建立单侧损毁... 目的:探讨核酸内切酶G(Endo-G)介导的非Caspase依赖性细胞凋亡在帕金森病(PD)发生发展中的作用和分子机制。方法:30只SPF级雄性SD大鼠均分为PD模型组(PD组)和对照组(Ctrl组),PD组大鼠右侧纹状体注射6-羟多巴胺(6-OHDA)诱导建立单侧损毁的PD大鼠模型,Ctrl组大鼠注射生理盐水;采用免疫组化实验观察大鼠黑质内酪氨酸羟化酶(TH)的变化以及核酸内切酶G(Endo-G)在黑质中的分布,计算Endo-G核转移细胞率;采用蛋白印迹实验(Western Bolt)检测Endo-G在黑质线粒体和细胞核中的表达量。结果:Ctrl组TH染色阳性神经元结构完整,PD模型组大鼠损毁侧黑质部位TH染色阳性细胞很难见完整的神经元结构;与Ctrl组比较,PD大鼠模型组损毁侧(右侧)黑质线粒体中Endo-G表达量明显降低(P<0.05),而细胞核中Endo-G表达量明显升高(P<0.05);Ctrl组大鼠Endo-G核转移细胞率低于PD组(P<0.05)。结论:在6-OHDA诱导的PD大鼠模型中,Endo-G自线粒体转位至细胞核,提示非Caspase依赖性细胞凋亡通路可能介导PD大鼠黑质多巴胺能神经元的变形和丢失。 展开更多
关键词 帕金森病 羟多巴胺 细胞凋亡 酪氨酸羟化酶 核酸内切酶G 非Caspase依赖性细胞凋亡
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PD98059联合紫杉醇对人胃印戒细胞癌细胞增殖和凋亡的影响 认领
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作者 赛福丁·柯尤木 布力布·吉力斯汉 +5 位作者 马兰英 李娜 阿布拉江·塔依尔 刘翠云 舍玲 唐勇 《中国药房》 CAS 北大核心 2020年第6期703-707,共5页
目的:探讨丝裂原激活蛋白激酶激酶/细胞外信号调节激酶(MEK/ERK)通路特异性抑制剂PD98059联合紫杉醇对人胃印戒细胞癌细胞增殖和凋亡的影响。方法:以人胃印戒细胞癌KATOⅢ细胞为对象,采用CCK-8法检测紫杉醇、PD98059以及两药联合作用48 ... 目的:探讨丝裂原激活蛋白激酶激酶/细胞外信号调节激酶(MEK/ERK)通路特异性抑制剂PD98059联合紫杉醇对人胃印戒细胞癌细胞增殖和凋亡的影响。方法:以人胃印戒细胞癌KATOⅢ细胞为对象,采用CCK-8法检测紫杉醇、PD98059以及两药联合作用48 h后的细胞增殖情况,并计算增殖抑制率;采用流式细胞术、Western blotting、Transwell法分别检测紫杉醇、PD98059以及两药联合作用48 h或24 h后的细胞凋亡、凋亡相关蛋白[分裂型胱天蛋白酶3(Cleaved-caspase-3)]表达和细胞迁移情况。结果:经紫杉醇(1μg/mL)、PD98059(5、20、40μmol/L)以及两药(1μg/mL+5、20、40μmol/L)联合作用后,各给药组细胞的增殖抑制率均显著升高,且联用组显著高于紫杉醇、PD98059同剂量单用组(P<0.05)。经紫杉醇(1μg/mL)、PD98059(40μmol/L)以及两药(1μg/mL+40μmol/L)联合作用后,紫杉醇组和两药联用组细胞的早期、晚期凋亡率以及Cleave-caspased-3蛋白的表达量均显著升高,且联用组显著高于紫杉醇、PD98059单用组(P<0.05);各给药组的细胞迁移数均显著减少,且联用组显著少于紫杉醇、PD98059单用组(P<0.05)。结论:紫杉醇、PD98059均可抑制人胃印戒细胞癌KATOⅢ细胞的增殖和迁移,且紫杉醇还可促进该细胞的凋亡及凋亡相关蛋白的表达,上述作用可能与抑制MEK/ERK通路有关。两药联用的效果优于紫杉醇或PD98059单用。 展开更多
关键词 人胃印戒细胞癌 紫杉醇 PD98059 增殖 凋亡 凋亡相关蛋白 迁移 丝裂原激活蛋白激酶激酶/细胞外信号调节激酶通路 KATOⅢ细胞
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Mkrn2 deficiency induces teratozoospermia and male infertility through p53/PERP-mediated apoptosis in testis 认领
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作者 Ying-Chen Qian Yun-Xia Xie +6 位作者 Chao-Shan Wang Zhu-Mei Shi Cheng-Fei Jiang Yun-Yi Tang Xu Qian Lin Wang Bing-Hua Jiang 《亚洲男性学杂志:英文版》 SCIE CAS CSCD 2020年第4期414-421,共8页
The apoptosis that occurs in the immature testis under physiological conditions is necessary for male germ cell development,whereas improper activation of apoptosis can impair spermatogenesis and cause defects in repr... The apoptosis that occurs in the immature testis under physiological conditions is necessary for male germ cell development,whereas improper activation of apoptosis can impair spermatogenesis and cause defects in reproduction.We previously demonstrated that in mice,the makorin-2(Mkrn 2)gene is expressed exclusively in the testis and its deletion leads to male infertility.To understand the potential molecular mechanism,in this study,we found that levels of apoptosis in the testis were abnormally high in the absence of Mkrn 2.To identify specific gene(s)involved,we performed digital gene expression profiling(DGE)and pathway analysis via gene set enrichment analysis(GSEA)and the Kyoto Encyclopedia of Genes and Genomes(KEGG)database,and we found that MKRN2 inhibits p53 apoptosis effector related to PMP22(PERP)expression and that levels of the protein in sperm samples have an inverse correlation with infertility levels.GSEA additionally indicated that PERP is a negative regulator of spermatogenesis and that its ectopic expression induces male infertility.Further,Gene Expression Omnibus(GEO)dataset analysis showed that p53,upstream of PERP,was upregulated in oligoasthenoteratozoospermia(OAT).These observations suggest that Mkrn 2 is crucial for protecting germ cells from excessive apoptosis and implicate Mkrn 2-based suppression of the p53/PERP signaling pathway in spermatogenesis and male fertility. 展开更多
关键词 APOPTOSIS makorin-2 P53 p53 apoptosis effector related to PMP22 spermatogenesis
牛磺酸诱导宫颈癌细胞凋亡的作用及可能机制 认领
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作者 梁笑倾 万福生 《实用癌症杂志》 2020年第10期1580-1584,共5页
目的观察牛磺酸(Tau)对宫颈癌细胞凋亡的影响及可能机制。方法培养宫颈癌HeLa细胞,采用四甲基偶氮唑盐(MTT)检测细胞增殖,流式细胞仪检测细胞凋亡,Western blot检测人哺乳动物不育系20样激酶1(MST1),Bcl-2及Bax蛋白表达。结果发现Tau能... 目的观察牛磺酸(Tau)对宫颈癌细胞凋亡的影响及可能机制。方法培养宫颈癌HeLa细胞,采用四甲基偶氮唑盐(MTT)检测细胞增殖,流式细胞仪检测细胞凋亡,Western blot检测人哺乳动物不育系20样激酶1(MST1),Bcl-2及Bax蛋白表达。结果发现Tau能诱导宫颈癌HeLa细胞凋亡和抑制增殖,并使HeLa细胞中MST1及Bax蛋白表达上调(P<0.01),Bcl-2蛋白表达水平下调(P<0.01);且过表达MST1能加强Tau对癌细胞凋亡的诱导作用(P<0.01)。结论牛磺酸对宫颈癌细胞凋亡有较强的诱导作用,其机制可能与牛磺酸能上调MST1及Bax蛋白表达有关。 展开更多
关键词 宫颈癌 牛磺酸 细胞凋亡 凋亡相关蛋白
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LncRNA DANCR调控非小细胞肺癌细胞的凋亡和上皮间质转化 认领
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作者 兰飞 赵鹏 +1 位作者 刘冬 张小燕 《现代医学》 2020年第1期75-82,共8页
目的:探讨促癌基因lncRNA DANCR在非小细胞肺癌(NSCLC)细胞的凋亡和上皮间质转化(EMT)中的分子机制。方法:培养NSCLC细胞系A549;对细胞使用siRNA沉默DANCR,qRT-PCR检测DANCR水平变化,Western blot检测DANCR靶基因FOXO1与其下游信号m TO... 目的:探讨促癌基因lncRNA DANCR在非小细胞肺癌(NSCLC)细胞的凋亡和上皮间质转化(EMT)中的分子机制。方法:培养NSCLC细胞系A549;对细胞使用siRNA沉默DANCR,qRT-PCR检测DANCR水平变化,Western blot检测DANCR靶基因FOXO1与其下游信号m TOR的表达;使用siRNA共沉默DANCR和FOXO1,Western blot检测FOXO1与其下游信号mTOR,VEGF,EMT诱导因子Twist1,EMT标记蛋白Ecadherin、vimentin的表达,Caspase3活性检测和cleaved-caspase3水平变化评估A549细胞的凋亡水平,Transwell细胞侵袭实验和ELISA检测外分泌VEGF水平变化评估细胞侵袭能力。结果:沉默DANCR显著性促进A549细胞中FOXO1和m TOR表达(P<0.05);与单独沉默DANCR相比,共沉默DANCR和FOXO1显著性减缓沉默DANCR对Caspase3活性和cleaved-caspase3水平的促进作用;沉默DANCR对细胞侵袭能力胞外VEGF和胞内VEGF表达、EMT诱导因子Twist1表达和EMT标记物的表达的抑制作用均被共沉默DANCR和FOXO1显著性逆转(P<0.05)。结论:LncRNA DANCR通过FOXO1/mTOR信号通路调节NSCLC的凋亡和EMT。 展开更多
关键词 非小细胞肺癌细胞 DANCR FOXO1/mTOR信号通路 细胞凋亡 上皮间质转化
石斛碱调节JNK信号通路对白血病细胞存活和上皮间质转化的影响 认领
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作者 郭涛 纪冬梅 +3 位作者 李艳平 卢阳 弋莉 王晓红 《广州中医药大学学报》 CAS 2020年第5期942-949,共8页
【目的】探讨石斛碱对体外培养的白血病细胞存活和转移特性的影响。【方法】用不同浓度石斛碱处理HuT-78细胞,选择无明显细胞毒性的浓度进行后续实验。以细胞计数盒8(CCK8)法测定细胞存活率;流式细胞术测定细胞凋亡水平;Transwell法测... 【目的】探讨石斛碱对体外培养的白血病细胞存活和转移特性的影响。【方法】用不同浓度石斛碱处理HuT-78细胞,选择无明显细胞毒性的浓度进行后续实验。以细胞计数盒8(CCK8)法测定细胞存活率;流式细胞术测定细胞凋亡水平;Transwell法测定细胞侵袭能力;蛋白免疫印迹(Western Blot)法检测细胞增殖、凋亡、上皮间质转化及c-Jun氨基末端激酶(JNK)信号通路蛋白表达水平。【结果】石斛碱浓度高于5μg/mL可对HuT-78细胞产生明显的细胞毒性;石斛碱剂量依赖性地抑制HuT-78细胞克隆数、上皮间质转化能力,促进细胞凋亡,并调节增殖、凋亡和上皮间质转化相关蛋白表达水平;且石斛碱能部分逆转JNK抑制剂SP600125对细胞增殖、凋亡和上皮间质转化相关蛋白表达水平的干预作用。【结论】石斛碱对白血病细胞存活和转移的抑制作用,与促JNK通路磷酸化激活有关。 展开更多
关键词 石斛碱 白血病 JNK信号通路 增殖 凋亡 上皮间质转化
敲减USP25对乳腺癌细胞生物学行为的影响 认领
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作者 荣欣欣 侯令密 +6 位作者 刘家有 李金穗 谢少利 杨懿 黄红梅 李静佳 邓世山 《川北医学院学报》 CAS 2020年第3期374-378,共5页
目的:探讨乳腺癌细胞中敲减泛素特异性蛋白酶25(USP25)后细胞生物学行为的改变。方法:采用慢病毒载体构建6条shRNA-USP25干扰序列(LV-shRNA-USP25-1~LV-shRNA-USP25-6),分别转染乳腺癌MCF-7细胞以干扰USP25的表达,并检测敲减效率,筛选... 目的:探讨乳腺癌细胞中敲减泛素特异性蛋白酶25(USP25)后细胞生物学行为的改变。方法:采用慢病毒载体构建6条shRNA-USP25干扰序列(LV-shRNA-USP25-1~LV-shRNA-USP25-6),分别转染乳腺癌MCF-7细胞以干扰USP25的表达,并检测敲减效率,筛选出最佳干扰序列用于实验。采用CCK8试剂盒法、Transwell侵袭实验、流式细胞术检测敲减USP25后乳腺癌细胞增殖、侵袭能力及凋亡的变化。结果:KD1组(转染LV-shRNA-USP25-1组)为干扰效率最高的序列,USP25蛋白和mRNA的敲减率分别为57.8%、58.3%(P<0.001);敲减USP25后乳腺癌MCF-7细胞增殖、侵袭能力受到抑制,且出现明显凋亡(P<0.001)。结论:USP25可能与乳腺癌细胞的增殖、侵袭及凋亡有密切关系,其可能在乳腺癌的恶性进展中扮演着重要角色。 展开更多
关键词 USP25 乳腺癌 细胞增殖 凋亡 侵袭
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灯盏乙素对缺血性心力衰竭大鼠心肌重构的影响及其机制 认领
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作者 张亚平 刘智 +3 位作者 段玉龙 赵军 范蒙蒙 刘玲 《广州中医药大学学报》 CAS 2020年第9期1761-1768,共8页
【目的】观察灯盏乙素对缺血性心力衰竭(IHF)大鼠心肌重构的影响及其机制。【方法】将90只大鼠随机分为假手术组,模型组,灯盏乙素低、中、高剂量组,阳性对照组,每组15只。除假手术组外,其他组别大鼠采用左前降支冠状动脉结扎方法建立IH... 【目的】观察灯盏乙素对缺血性心力衰竭(IHF)大鼠心肌重构的影响及其机制。【方法】将90只大鼠随机分为假手术组,模型组,灯盏乙素低、中、高剂量组,阳性对照组,每组15只。除假手术组外,其他组别大鼠采用左前降支冠状动脉结扎方法建立IHF模型。从造模第3天开始至8周末,灯盏乙素低、中、高剂量组大鼠给予腹腔注射灯盏乙素(剂量分别为0.3、3、30 mg·kg-1·d-1),阳性对照组大鼠给予卡托普利(180 mg·kg-1·d-1)灌胃,假手术组和模型组大鼠给予腹腔注射等量生理盐水。给药结束后,检测血压、心率和超声心动相关指标[射血分数(EF)、收缩分数(FS)、舒张早期二尖瓣血流速度/舒张晚期二尖瓣血流速度(E/A)比值,心室舒张末期室间隔厚度(IVSd)、左心室舒张末期容积(LVEDV)、左心室收缩末期容积(LVESV)、左心室舒张末期直径(LVIDd)、左心室收缩末期直径(LVIDs)],苏木素-伊红(HE)染色观察心肌病理改变,流式细胞术检测心肌细胞凋亡,蛋白免疫印迹(Western Blot)法检测心肌细胞凋亡标志蛋白裂解半胱氨酸天冬氨酸蛋白酶3(cleaved Caspase-3)、Bax-Bcl-2,心肌重构相关蛋白胶原蛋白(Collagin)Ⅰ、CollaginⅢ、基质金属蛋白酶(MMP)-1、MMP-2和MMP-9的表达水平,酶联免疫吸附分析(ELISA)检测心肌中炎症因子白细胞介素(IL)-18、IL-1β、IL-6、细胞间粘附分子-1(ICAM-1)、肿瘤坏死因子α(TNF-α)含量。【结果】与模型组比较,灯盏乙素低、中、高剂量组大鼠收缩压、舒张压和心率及EF、FS、E/A明显提高,LVEDV、LVESV、LVIDd、LVIDs降低,心肌损伤减轻,心肌细胞凋亡率,cleaved Caspase-3、Bax/Bcl-2蛋白表达水平降低,CollagenⅠ、CollaginⅢ、MMP-1、MMP-2和MMP-9表达水平降低,IL-18、IL-1β、ICAM-1、TNF-α含量降低,其中灯盏乙素高剂量组作用差异有统计学意义(P<0.05),IVSd与IL-6含量无明显改变(P>0.05)。【结论】灯盏乙素可改善IHF大鼠血压� 展开更多
关键词 灯盏乙素 缺血性心力衰竭 心肌重构 凋亡 炎症反应 大鼠
骨髓造血干祖细胞改善慢性约束应激诱导的小鼠脾细胞数减少 认领
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作者 付慧 常芬 +2 位作者 王浩玉 白芃 康杰 《山西医科大学学报》 CAS 2020年第3期231-236,共6页
目的观察CD34+骨髓造血干祖细胞(CD34+HSPC)对慢性约束应激小鼠脾细胞数的影响。方法将10只8周龄雄性BALB/c小鼠分为2组(n=5):①慢性应激组:小鼠放入约束应激管中约束12 h/d(早9:00-晚9:00),解除约束12 h/d(晚9:00-早9:00),连续处理3 d... 目的观察CD34+骨髓造血干祖细胞(CD34+HSPC)对慢性约束应激小鼠脾细胞数的影响。方法将10只8周龄雄性BALB/c小鼠分为2组(n=5):①慢性应激组:小鼠放入约束应激管中约束12 h/d(早9:00-晚9:00),解除约束12 h/d(晚9:00-早9:00),连续处理3 d以建立慢性约束应激的小鼠模型;②对照组:正常饲养不施加任何处理。慢性应激第3天结束时即取每组小鼠脾并计数脾细胞。HSPC体内干预实验中,20只雄性BALB/c小鼠分为4组(n=5):HSPC干预+慢性应激组,溶剂对照+慢性应激组,HSPC干预组和溶剂对照组。HSPC干预+慢性应激组和溶剂对照+慢性应激组慢性应激第3天结束时即取每组小鼠脾并计数脾细胞,流式细胞术检测其中活细胞、凋亡细胞及坏死细胞比例。绿色荧光标记HSPC做体内示踪试验,检测迁移至脾的HSPC。HSPC体外干预实验中,细胞培养分为4组:HSPC干预+地塞米松组,脾细胞+地塞米松组,HSPC干预组和脾细胞单独培养组,培养18 h,流式细胞术检测其中活细胞、凋亡细胞及坏死细胞的比例。结果脾细胞计数结果表明,与对照组相比,慢性应激组小鼠的脾细胞总数显著减少(P<0.05)。HSPC体内干预实验中,与溶剂对照+慢性应激组相比,HSPC干预+慢性应激组小鼠脾细胞计数增加(P<0.05)。流式细胞术结果表明,与溶剂对照组相比,溶剂对照+慢性应激组小鼠脾细胞凋亡及坏死比例增加(P<0.05);与溶剂对照+慢性应激组相比,HSPC干预+慢性应激组小鼠脾细胞凋亡比例减少,活细胞比例增加(P<0.05)。体内示踪试验结果显示,慢性应激过程中HSPC可迁移至脾中。体外实验结果表明,与脾细胞单独培养组相比,脾细胞+地塞米松组脾细胞凋亡及坏死比例增加(P<0.05);与脾细胞+地塞米松组相比,HSPC干预+地塞米松组脾细胞坏死比例减少,活细胞比例增加(P<0.05)。结论CD34+HSPC可改善慢性约束应激诱导的小鼠脾细胞数的减少。 展开更多
关键词 造血干祖细胞 慢性约束应激 脾细胞 细胞凋亡 细胞坏死 小鼠
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