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1.
目的:研究胡桃醌诱导人乳腺癌MCF-7细胞凋亡及其形态学观察。方法:四甲基偶氮唑蓝(MTT)法检测胡桃醌对MCF-7细胞的增殖抑制作用;Hochest33258荧光染色法观察细胞凋亡形态;流式细胞术(FCM)检测细胞凋亡率。结果:胡桃醌对人乳腺癌MCF-7细胞的IC50为11.99μmol/L;胡桃醌作用24h后,细胞生长密度变疏,细胞皱缩,出现凋亡小体,且随着给药浓度升高,凋亡小体也逐渐增多;胡桃醌5、10、20μmol/L作用24h后MCF-7细胞凋亡率分别为6.35%、12.43%、28.55%。结论:胡桃醌对人乳腺癌MCF-7细胞具有增殖抑制作用。 相似文献
2.
目的:研究大蒜素对人肝癌HepG2细胞生长的抑制作用。方法:体外培养人肝癌HepG2细胞,形态学观察大蒜素作用下HepG2细胞的生长变化,四甲基偶氮唑蓝(MTT)比色法检测实验各组HepG2细胞的生长增殖情况。结果:形态学观察显示,在大蒜素作用下,HepG2细胞失去原有"铺路石"样排列,细胞间连接减少或消失,细胞黏附性下降,出现细胞凋亡特征;MTT比色法检测发现,不同浓度的大蒜素均能抑制肝癌细胞的生长(P<0.05),且呈剂量依赖性。结论:大蒜素对人肝癌HepG2细胞的生长起一定的抑制作用。 相似文献
3.
[目的]建立流式细胞术分析肿瘤细胞内阿霉素分布的方法,并研究低浓度五味子乙素对K562细胞内化阿霉素的影响。[方法]体外培养猪内皮细胞(pEC),以20μmol/L阿霉素处理2、4和6小时;或加入不同浓度阿霉素(0、10、20、40、80和100μmol/L)处理4小时。培养K562细胞,以5μmol/L阿霉素处理2、4和6小时;或加入不同浓度阿霉素(0、2.5、5、10和20μmol/L)处理4小时。采用不同浓度(0、25、50和100μmol/L)五味子乙素(Sch B)与阿霉素联合处理K562细胞4小时。收集细胞,采用流式细胞术分析阿霉素的特异荧光。[结果]固定浓度处理pEC(20μmol/L)和K562(5μmol/L)后检测,发现细胞内荧光强度随时间延长而增加,两种细胞4小时组荧光强度分别达到6小时组的96.93%和95.23%/。在直方图上,阴性和阳性细胞群界限分明。阿霉素(2.5、5和10μmol/L)单独处理细胞的荧光强度分别为26.78±3.34、64.70±6.24和118.35±9.67;添加25μmol/L Sch B实验后荧光强度增加到43.45±4.25、103.74±7.36和146.69±8.32,Sch B显著增加了K562细胞内阿霉素的分布(p<0.05)。[结论]建立的方案可快速测定细胞内的阿霉素分布;低浓度Sch B促进肿瘤细胞内化阿霉素。 相似文献
4.
目的:观察异鼠李素对鼻咽癌CNE-1细胞生长及增殖的抑制作用。方法:用不同浓度(10、30、50、70、90μg/m L)的异鼠李素处理人鼻咽癌CNE-1细胞,在不同时间点分别采用CCk-8法检测测细胞生长抑制率;台盼蓝染色测细胞活力;平皿培养测细胞集落形成能力。结果:与正常组相比,异鼠李素处理CNE-1细胞48h后,细胞生长抑制率明升高(p0.05或p0.01);用药物处理细胞6d,随着时间的延长,细胞生长活力逐渐降低;药物处理7天后,药物处理组细胞集落形成能力明显低于正常组(p0.05或p0.01)且以上方法都显示在一定范围内,异鼠李素对CNE-1细胞的生长及增殖抑制作用呈剂量依赖性。结论:异鼠李素可明显抑制鼻咽癌CNE-1细胞的生长和增殖。 相似文献
5.
阿尔茨海默病(AD)是最常见的与年龄有关的神经退行性疾病.全世界约15%的65岁以上人群和30%的80岁以上老人患有AD.AD的病因仍未明确,目前尚无有效的预防和治疗方法.随着人类社会的老龄化,本病已成为一个世界性的重大医学和社会难题.许多证据显示β-淀粉样肽在阿尔茨海默病(AD)的病因学和/或病程发展中起着关键作用.很多研究提示β-淀粉样肽的神经毒性与氧的负荷和自由基损伤密切相关.最近的研究表明,NF-κB在神经元存活和突触的可塑性方面发挥重要作用,CREB是长时程记忆(LTM)和长时程增强效应(LTP)的必要基因开关.本研究观察了科研新药ECH-931对β-淀粉样肽1～40,β-淀粉样肽25～35和H202所诱导的B104中枢神经系神经元细胞株神经毒性的预防和治疗作用.ECH-931的低,中,高实验浓度分别为50μg/mi,100μg/mi和150/200μg/mi,用ECH-931处理的方案如下细胞经ECH-931预处理3天后,用ECH-931和H202(100～200μM)共同处理3～12小时,以观察ECH-931对H202神经毒性的防治效果;细胞经ECH-931预处理3天后,用ECH-931和Abeta 1～40(10μM)处理48小时来预防性治疗Abeta1～40的神经毒性;在细胞暴露于Abeta25～35(25μM)8小时后再用ECH-931处理48小时(经ECH-931和Abeta25～35共同处理48小时)以观察ECH-931对Abeta神经毒性的治疗作用在NF-κB和CREB基因转染后以ECH-931处理5天,以观察ECH-931对NF-κ B和CREB基因表达的影响;在NF-κB基因转染并加Abeta1～40(5μM)后以ECH-931处理3天,以观察ECH-931拮抗Abeta1～40对NF-κB基因表达影响的效果.结果表明经ECH-931(50～200μg/mi)预处理和共同处理B104神经元能完全拮抗β-淀粉样肽1～40(10μM)诱导的神经毒性(P〈0.05～0.01〉;用ECH-931(50～200μg/mi)治疗性处理能显著阻止由β-淀粉样肽25～35(25μM)诱导的B104神经元细胞死亡/凋亡(P＜0.05～0.01);用ECH-931(50～200μg/mi)预处理和共同处理能显著保护由H202(100～200μM)诱导的B104神经元细胞死亡/凋亡;用ECH-931(50～150μg/mi)治疗性处理能显著上调在B104 CNS神经元细胞中转染基因NF-κB和CREB的表达(P〈0.05～0.01〉;ECH-93150～150μg/mi能拮抗由β-淀粉样肽1～40诱导的NF-κB表达抑制(P〈0.01〉.并且,所有ECH-931的处理效应都呈现剂量依赖性(P＜0.05～0.01).基于以上研究结果,我们认为ECH-931能保护(预防和治疗)神经元免受由β-淀粉样肽诱导的神经毒性.其机制与拮抗活性氧/氢氧根自由基损伤和激活NF-κB细胞存活信号通路有关.ECH-931治疗AD的另一个重要机理可能是它能调节CREB的表达,而CREB是长期记忆的基因开关.ECH-931的神经元保护效应尤其是其阻止β-淀粉样肽诱导的毒性和细胞死亡的效力显示出它治疗神经退行性疾病(如AD)的潜力,具有重要的研究开发价值和广阔的应用前景. 相似文献
6.
阿尔茨海默病(AD)是最常见的与年龄有关的神经退行性疾病.全世界约15%的65岁以上人群和30%的80岁以上老人患有AD.AD的病因仍未明确,目前尚无有效的预防和治疗方法.随着人类社会的老龄化,本病已成为一个世界性的重大医学和社会难题.许多证据显示β-淀粉样肽在阿尔茨海默病(AD)的病因学和/或病程发展中起着关键作用.很多研究提示β-淀粉样肽的神经毒性与氧的负荷和自由基损伤密切相关.最近的研究表明,NF-κB在神经元存活和突触的可塑性方面发挥重要作用,CREB是长时程记忆(LTM)和长时程增强效应(LTP)的必要基因开关.本研究观察了科研新药ECH-931对β-淀粉样肽1～40,β-淀粉样肽25～35和H202所诱导的B104中枢神经系神经元细胞株神经毒性的预防和治疗作用.ECH-931的低,中,高实验浓度分别为50μg/mi,100μg/mi和150/200μg/mi,用ECH-931处理的方案如下:细胞经ECH-931预处理3天后,用ECH-931和H202(100～200μM)共同处理3～12小时,以观察ECH-931对H202神经毒性的防治效果;细胞经ECH-931预处理3天后,用ECH-931和Abeta 1～40(10μM)处理48小时来预防性治疗Abeta1～40的神经毒性;在细胞暴露于Abeta25～35(25μM)8小时后再用ECH-931处理48小时(经ECH-931和Abeta25～35共同处理48小时)以观察ECH-931对Abeta神经毒性的治疗作用:在NF-κB和CREB基因转染后以ECH-931处理5天,以观察ECH-931对NF-κ B和CREB基因表达的影响;在NF-κB基因转染并加Abeta1～40(5μM)后以ECH-931处理3天,以观察ECH-931拮抗Abeta1～40对NF-κB基因表达影响的效果.结果表明:经ECH-931(50～200μg/mi)预处理和共同处理B104神经元能完全拮抗β-淀粉样肽1～40(10μM)诱导的神经毒性(P〈0.05～0.01〉;用ECH-931(50～200μg/mi)治疗性处理能显著阻止由β-淀粉样肽25～35(25μM)诱导的B104神经元细胞死亡/凋亡(P＜0.05～0.01);用ECH-931(50～200μg/mi)预处理和共同处理能显著保护由H202(100～200μM)诱导的B104神经元细胞死亡/凋亡;用ECH-931(50～150μg/mi)治疗性处理能显著上调在B104 CNS神经元细胞中转染基因NF-κB和CREB的表达(P〈0.05～0.01〉;ECH-93150～150μg/mi能拮抗由β-淀粉样肽1～40诱导的NF-κB表达抑制(P〈0.01〉.并且,所有ECH-931的处理效应都呈现剂量依赖性(P＜0.05～0.01).基于以上研究结果,我们认为ECH-931能保护(预防和治疗)神经元免受由β-淀粉样肽诱导的神经毒性.其机制与拮抗活性氧/氢氧根自由基损伤和激活NF-κB细胞存活信号通路有关.ECH-931治疗AD的另一个重要机理可能是它能调节CREB的表达,而CREB是长期记忆的基因开关.ECH-931的神经元保护效应尤其是其阻止β-淀粉样肽诱导的毒性和细胞死亡的效力显示出它治疗神经退行性疾病(如AD)的潜力,具有重要的研究开发价值和广阔的应用前景. 相似文献
7.
研究RNA干扰EGFR表达对鼻咽癌CNE2细胞的细胞周期趋势的影响.利用携带EGFR小发夹干扰RNA(small hairpin RNA shRNA)的重组表达载体,脂质体法染到CNE2细胞.流式细胞仪检测鼻咽癌CNE2细胞在EGFR沉默后在细胞各期的细胞比例和增殖指数,吉姆萨染色检测细胞的形态学变化.实验EGFR沉默后的鼻咽癌CNE2细胞周期分布发生明显的改变,与对照组和空白组对比.G0/G1和G2/M期细胞比例和凋亡率明显增加.而S期细胞比例显著降低;凋亡率显著升高.结论:靶向干扰EGFR可抑制鼻咽癌CNE2细胞增植,并诱导其凋亡. 相似文献
8.
目的研究新疆紫草的提取物紫草素抑制B细胞非霍奇金淋巴瘤生长能力。方法对体外培养的Raji细胞PI染色,并进行荧光显微镜观察,同时,采用中性红染色的方法检测细胞在不同浓度紫草素作用下的存活率。结果紫草素对Raji细胞生长有抑制作用,能够诱导Raji细胞死亡,并呈浓度依赖。结论紫草素可以抑制Raji生长,对B细胞非霍奇金淋巴瘤的治疗有重要作用。 相似文献
9.
以16个水稻品种为材料，测定了铜对水稻种子萌发相关指标，并观察了根尖有丝分裂及分生区Ca分布的影响。结果表明：（1）0．1mM和0．2mMCuSO4溶液处理对水稻根长的抑制作用大于对芽长的抑制，且对不同品种根长的抑制作用存在明显差异；（2）随着铜处理浓度（25、50、75、100μM）的升高，根尖细胞有丝分裂指数及相对有丝分裂指数皆呈下降趋势；（3）t常生长条件下，水稻根尖分生区细胞中的Ca主要分布在液泡和细胞间隙中，而细胞质、细胞核中分布很少；50μM铜处理下，根尖分生区细胞液泡和胞间的Ca沉淀颗粒明显减少，而胞质及核基质中的Ca沉淀颗粒增多。铜胁迫造成根尖细胞中原有Ca分布的变化可能是引起细胞功能的紊乱，进而影响根系生长的原因之一。 相似文献
10.
《黑龙江科技信息》2016,(5)
目的:考察逍遥散中所含的伞形花内酯、阿魏酸和柴胡皂苷d三种类植物雌激素成分对MCF-7乳腺癌细胞增殖的影响。方法:利用体外培养的ER阳性人乳腺癌细胞系MCF-7细胞,采用MTT法测定对MCF-7细胞增殖的影响。结果:伞形花内酯(100μmol/L)、阿魏酸(100μmol/L)、柴胡皂苷d(100μmol/L)、均可显著抑制MCF-7细胞的增殖(P0.05),对细胞有毒性作用,不适合用于下一步的实验研究,其他药物浓度对细胞增殖无明显影响。结论:伞形花内酯、阿魏酸、柴胡皂苷d能抑制细胞增殖可能是其发挥了抗雌激素样作用,但其发挥作用的机制还有待于深入研究。 相似文献
11.
Shaymaa M. M. Yahya Shadia A. Fathy Zakaria A. El-Khayat Safinaz E. El-Toukhy Ahmed R. Hamed Marwa G. A. Hegazy Heba K. Nabih 《Indian journal of clinical biochemistry : IJCB》2018,33(1):21-30
Hepatocellular carcinoma (HCC) is a hypervascular primary liver cancer characterized by rapid progression, besides, resistance to traditional chemotherapeutic agents. It has been shown that microRNAs play critical roles in regulation of tumor cell sensitivity to drugs through modulating the expression of genes involved in drug transport. The present study investigated whether restoration of miR-122 in HCC cells could alter the cell cycle distribution and the expression of multidrug resistance (MDR)-related genes (ABCB1, ABCC1, ABCG2 and ABCF2). After overexpression of miR-122 in HepG2 cells treated or untreated with doxorubicin doses, total RNAs and protein extracts were isolated for application of QRT-PCR and western blotting techniques. Moreover, cell cycle distribution was monitored by flow cytometry. Our results revealed that, the over expression of miR-122 in HepG2 cells treated or untreated with doxorubicin could modulate the sensitivity of cells to chemotherapeutic drug through downregulation of MDR-related genes, ABCB1 and ABCF2. Interpretation of cell cycle distribution revealed that, the anti-proliferative effect of miR-122 is associated with the accumulation of cells in G0/G1 phase. Moreover, treatment with miR-122 and doxorubicin resulted in high percentage of HCC cells in G0/G1 phase. Taken together, our findings revealed that, overexpression of miR-122 inhibited HCC cell growth by inducing cell cycle arrest and this arrest is associated with down-regulation of MDR-related genes. 相似文献
12.
BackgroundTo reduce costs associated with productivity of recombinant proteins in the biopharmaceutical industry, research has been focused on regulatory principals of growth and survival during the production phases of the cell culture. The main strategies involve the regulation of cell proliferation by the modulation of cell cycle control points (G1/S or G2/M) with mild hypothermia and the addition of sodium butyrate (NaBu). In this study, batch culture strategies were evaluated using CHO TF 70R cells producing the recombinant human tissue plasminogen activator (rh-tPA), to observe their individual and combined effect on the cellular physiological state and relevant kinetic parameters.ResultsNaBu addition has a negative effect on the mitochondrial membrane potential (∆ Ψm), the values of which are remarkably diminished in cultures exposed to this cytotoxic compound. This effect was not reflected in a loss of cell viability. NaBu and mild hypothermic conditions increased the doubling time in the cell cultures, suggesting that these strategies triggered a general slowing of each cell cycle phase in a different way. Finally, the individual and combined effect of NaBu and mild hypothermia produced an increase in the specific rh-tPA productivity in comparison to the control at 37°C without NaBu. Nevertheless, both strategies did not have a synergistic effect on the specific productivity.ConclusionsThe combination of NaBu addition and mild hypothermic condition causes an impact on physiological and metabolic state of CHO TF 70R cells, decreasing cell growth rate and improving glucose consumption efficiency. These results therefore provide a promising strategy to increase specific productivity of rh-tPA. 相似文献
13.
通过对μC／OS～Ⅱ实时操作系统和GUI图形界面在S3C44BOX上的移植,可以实现系统启动加栽Bootloader、μC／OS～Ⅱ操作系统的移植、串口程序的通讯、GUI图形界面的应用等功能,使系统软件平台的设计与应用范围有较大的拓展。 相似文献
14.
AIM To filtrate breast cancer resistance protein(BCRP)-mediated resistance agents and investigate the mechanism,so as to provide valuable datum for optimization clinical chemotherapy scheme to tumor with evaluation marker of BCRP expression. METHODS MTT assay was used to filtrate BCRP-mediated resistance agents with PA317/Tet-on/TRE-BCRP cell of different expression levels of BCRP after treated with different concentration anticancer agents. High performance liquid chromatography(HPLC) was applied to measure relative dose of intracellular retention resistance agents. Nuclear DNA fluorescence dye,Hochest 33258, staining and flow cytometry were adopted to detect apoptotic cells after treated with drugs. RESULTS There were shown increasing durg-resistance to 5-fluorouracil,methotrexate, doxirubicin, pirarubicin,etoposide and mitoxantrone followed with increasing expression of BCRP on PA317/Tet-on/TRE-BCRP cells(P＜0.05, n=3),but shown sensitive to paclitaxel, cisplatin, vincristine, mitomycin and vindesine. There also was shown significant negative correlation between the intracellular retention dose of 5-fluorouracil with different expression of BCRP(r=-0.885, P＜0.05, n=3).There were shown parallel results of that decreasing cellular apoptotic rate with increasing cellular expression of BCRP after treated with 5-fluorouracil by fluorescence dye staining and flow cytometry(P＜0.05, n=3),and also shown significate rise of the apoptotic rate of BCRP expression cells after treated with Ko143 (P＜0.05, n=3). Every group of cells could be different extently blocked in phase of G0/G1 treated with 5-fluorouracil. CONCLUSION Resistance of 5-fluorouracil could be especially mediated by conjugated with BCRP and acted as drug exclude-pump substrate. Cellular ability resistant to 5-fluorouracil-induced apoptosis could be reinforced by BCRP expression. 相似文献
15.
Azim Akbarzadeh Dariush Norouzian Ali Farhangi Mohammad Reza Mehrabi Shirin Jamshidi Davood Zare Morvarid Shafiei 《Indian journal of clinical biochemistry : IJCB》2008,23(1):57-61
Flow cytometry has been employed as a method to study homogeneity of isolated islet subpopulations. After collagenase digestion
of rat pancreas and elutriation of tissue fragments, islets were isolated and dissociated, and cells were analyzed and sorted
according to their low forward angle light scattering properties by using automated flow cytometry. A standardized procedure
was developed for the preparation of rat islet cell grafts for purification of islet cells. In this process, after collagenase
digestion of pancreas, islets were isolated, dissociated, identification by dithizone method and then with enzymatic procedure
by DNase and trypsin, the islet cells changed into single cells and beta cells were identified by immunofluorescence method
and then assayed by flow cytometry. Methods have been developed for the preparation of suspension of viable rat pancreatic
islet cells and their analysis and sorting in the fluorescence activated cell sorter (FACC IV, Becton Dickinson, Sunnyvale,
Ca). Flow cytometry of these cells indicated that there were 91% of beta cells in cell suspension. Most of the exocrine particles
were lost during digestion. Purified endocrine islet cell grafts were prepared by pure beta-cells, without endocrine non-beta
cells. The purified aggregates were devoid of endocrine non-beta cells and damaged cells. 相似文献
16.
In the present study, the effect of red (Gracillaria corticata), green (Ulva fasciata) and brown (Sargassum ilicifolium) seaweeds alcoholic extract, against five important human cancer cell lines (MCF-7, MDA-MB-231, HeLa, HepG2, and HT-29) proliferation, apoptosis and cell cycle arrest were evaluated. The reducing activity and total polyphenol content were also investigated. MTT assay was used for cytotoxicity test. Morphological alterations were examined using phase contrast, fluorescent and electron microscopy. All the extracts were antiproliferative against all the cancer cell lines, dose-dependently, with G. corticata methanol extract (GCME) having the greatest inhibition activity against MCF-7 cell line. The percentage of apoptosis increased from 18 to 78 %. The cell cycle analysis also showed that GCME can induce apoptosis which confirm by TEM. Algal extract reducing activities were as follows: G. corticata > S. ilicifolium > U. fasciata. The GCME is a good source of potential complementary and alternative functional food for prevention and treatment of cancer. 相似文献
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目的探讨氯化铵(NH4CL)对顺铂(cisplatin,CDDP)抑制A549细胞增殖的影响。方法体外培养人肺癌A549细胞,MTT法检测NH4CL及CDDP对人肺癌A549细胞增殖率的影响;光镜下观察NH4CL及CDDP对A549细胞生长的影响;共聚焦显微镜下观察A549细胞核的形态变化。结果与对照组相比,给予不同浓度的NH4CL及CDDP导致A549细胞增殖率明显下降;光镜下观察A549细胞经非毒性剂量的NH4CL与CDDP联合应用处理后细胞生长抑制明显高于单独给予CDDP组;共聚焦显微镜观察可见非毒性剂量的NH4CL与CDDP联合应用处理A549细胞核碎裂现象明显多于单独CDDP处理组。结论 NH4CL可以促进CDDP对A549A细胞的凋亡诱导作用。 相似文献
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Chao Wei Beiyuan Fan Deyong Chen Chao Liu Yuanchen Wei Bo Huo Lidan You Junbo Wang Jian Chen 《Biomicrofluidics》2015,9(1)
This paper presents a microfluidic device (poly-dimethylsiloxane micro channels bonded with glass slides) enabling culture of MLO-Y4 osteocyte like cells. In this study, on-chip collagen coating, cell seeding and culture, as well as staining were demonstrated in a tubing-free manner where gravity was used as the driving force for liquid transportation. MLO-Y4 cells were cultured in microfluidic channels with and without collagen coating where cellular images in a time sequence were taken and analyzed, confirming the positive effect of collagen coating on phenotype maintaining of MLO-Y4 cells. The proliferating cell nuclear antigen based proliferation assay was used to study cellular proliferation, revealing a higher proliferation rate of MLO-Y4 cells seeded in microfluidic channels without collagen coating compared to the substrates coated with collagen. Furthermore, the effects of channel dimensions (variations in width and height) on the viability of MLO-Y4 cells were explored based on the Calcein-AM and propidium iodide based live/dead assay and the Hoechst 33258 based apoptosis assay, locating the correlation between the decrease in channel width or height and the decrease in cell viability. As a platform technology, this microfluidic device may function as a new cell culture model enabling studies of osteocytes. 相似文献