期刊文献+
共找到299篇文章
< 1 2 15 >
每页显示 20 50 100
青藤碱调节CXCR4-STAT3轴对卵巢癌A2780细胞增殖、迁移和血管生成拟态的影响
1
作者 闫振宇 郭锰 +2 位作者 杨然 苏博 张海燕 《现代肿瘤医学》 CAS 2024年第16期2944-2951,共8页
目的:探讨青藤碱(Sinomenine)对卵巢癌细胞增殖、迁移和血管生成拟态的影响及作用机制。方法:使用不同浓度(0、0.25、0.50、1.0、2.0、4.0、8.0 mmol/L)的青藤碱分别处理A2780细胞24、48 h, CCK-8法检测细胞存活率。将A2780细胞随机分... 目的:探讨青藤碱(Sinomenine)对卵巢癌细胞增殖、迁移和血管生成拟态的影响及作用机制。方法:使用不同浓度(0、0.25、0.50、1.0、2.0、4.0、8.0 mmol/L)的青藤碱分别处理A2780细胞24、48 h, CCK-8法检测细胞存活率。将A2780细胞随机分为对照(Control)组、CXCR4激活剂基质细胞衍生因子-1(SDF-1)(SDF-1,100 ng/mL)组、CXCR4抑制剂普乐沙福(Plerixafor, 500 ng/mL)组、青藤碱(Sinomenine, 1.0 mmol/L)组、Sinomenine+SDF-1(1.0 mmol/L Sinomenine+100 ng/mL SDF-1)组,分别检测A2780细胞增殖、迁移与侵袭,体外血管生成拟态形成实验检测青藤碱对血管生成拟态的影响,Western blot法检测血管内皮生长因子(VEGF)、上皮细胞激酶(EphA2)、基质金属蛋白酶9(MMP-9)、MMP-2、CXC趋化因子受体4(CXCR4)、信号转导与转录激活因子3(STAT3)、磷酸化STAT3(p-STAT3)蛋白表达。结果:青藤碱可有效抑制A2780细胞增殖,且呈浓度依赖性;青藤碱可显著抑制A2780细胞迁移、侵袭及血管生成拟态形成,并下调血管生成拟态标志蛋白VEGF、EphA2、MMP-9、MMP-2表达,抑制CXCR4、p-STAT3表达(P<0.05),青藤碱的这一抑制作用可被CXCR4激活剂减弱。结论:青藤碱可能通过抑制CXCR4-STAT3轴,抑制卵巢癌细胞增殖、迁移、侵袭及血管生成拟态形成。 展开更多
关键词 青藤碱 CXC趋化因子受体4-信号转导与转录激活因子3轴 卵巢癌细胞 增殖 迁移 血管生成拟态
下载PDF
miR-409-3p通过靶向脂肪酸结合蛋白4影响子宫内膜癌细胞转移的研究
2
作者 张雨 刘芳 《成都医学院学报》 CAS 2024年第4期603-609,共7页
目的用生物信息学方法预测脂肪酸结合蛋白4(FABP4)的上游调控miRNA,体外培养子宫内膜癌细胞Ishikawa,了解微小核糖核酸-409-3p(miR-409-3p)是否通过抑制FABP4的表达水平,进而影响Ishikawa细胞的生物学行为。方法实验分为control组、miR-... 目的用生物信息学方法预测脂肪酸结合蛋白4(FABP4)的上游调控miRNA,体外培养子宫内膜癌细胞Ishikawa,了解微小核糖核酸-409-3p(miR-409-3p)是否通过抑制FABP4的表达水平,进而影响Ishikawa细胞的生物学行为。方法实验分为control组、miR-409-3p mimics组、miR-409-3p inhibitor组、miR-409-3p NC组、FABP4-OE组及FABP4-shRNA组6组,采用实时定量聚合酶链式反应及蛋白质印迹法检测miR-409-3p及FABP4在Ishikawa中的表达情况;采用细胞增殖实验(CCK-8)、细胞侵袭及迁移实验(Transwell法)检测miR-409-3p与FABP4对Ishikawa细胞增殖、侵袭以及迁移能力的影响;用双荧光素酶报告基因实验在Ishikawa细胞中检测miR-409-3p对FABP4的调控作用。结果1)在Ishikawa细胞中下调FABP4的表达后,Ishikawa细胞的增殖、侵袭和迁移能力均显著降低(P<0.05);在Ishikawa细胞中上调FABP4的表达后,Ishikawa细胞的增殖、侵袭和迁移能力均显著升高(P<0.05)。2)在Ishikawa细胞中转染miR-409-3p mimics后,FABP4的表达水平以及Ishikawa细胞的增殖、侵袭和迁移能力均显著降低(P<0.05);而转染miR-409-3p inhibitor后,FABP4的表达水平以及Ishikawa细胞的增殖、侵袭和迁移能力均显著升高(P<0.05)。3)双荧光素酶报告基因结果显示,在Ishikawa细胞中miR-409-3p可靶向调控FABP4。结论高表达的FABP4促进Ishikawa细胞增殖、侵袭及迁移,miR-409-3p可通过下调FABP4的表达进而抑制Ishikawa细胞发生转移。 展开更多
关键词 子宫内膜癌细胞 FABP4 miR-409-3p 增殖 侵袭 迁移
下载PDF
Chemokine platelet factor 4 accelerates peripheral nerve regeneration by regulating Schwann cell activation and axon elongation 被引量:1
3
作者 Miao Gu Xiao Cheng +3 位作者 Di Zhang Weiyan Wu Yi Cao Jianghong He 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第1期190-195,共6页
Schwann cells in peripheral nerves react to traumatic nerve injury by attempting to grow and regenerate.Howeve r,it is unclear what factors play a role in this process.In this study,we searched a GEO database and foun... Schwann cells in peripheral nerves react to traumatic nerve injury by attempting to grow and regenerate.Howeve r,it is unclear what factors play a role in this process.In this study,we searched a GEO database and found that expression of platelet factor 4 was markedly up-regulated after sciatic nerve injury.Platelet factor is an important molecule in cell apoptosis,diffe rentiation,survival,and proliferation.Further,polymerase chain reaction and immunohistochemical staining confirmed the change in platelet factor 4 in the sciatic nerve at different time points after injury.Enzyme-linked immunosorbent assay confirmed that platelet factor 4 was secreted by Schwann cells.We also found that silencing platelet factor 4 decreased the proliferation and migration of primary cultured Schwann cells,while exogenously applied platelet factor 4 stimulated Schwann cell prolife ration and migration and neuronal axon growth.Furthermore,knocking out platelet factor 4 inhibited the prolife ration of Schwann cells in injured rat sciatic nerve.These findings suggest that Schwann cell-secreted platelet factor 4 may facilitate peripheral nerve repair and regeneration by regulating Schwann cell activation and axon growth.Thus,platelet factor 4 may be a potential therapeutic target for traumatic peripheral nerve injury. 展开更多
关键词 axon elongation bioinformatic analysis cell migration cell proliferation dorsal root ganglia peripheral nerve regeneration peripheral nerve trauma platelet factor 4 rat sciatic nerve Schwann cells
下载PDF
Migration of Infiltrated NH_4 and NO_3 in a Soil and Groundwater System Simulated by a Soil Tank 被引量:1
4
作者 WANG Chao WANG Pei-Fang 《Pedosphere》 SCIE CAS CSCD 2008年第5期628-637,共10页
The infiltration of water contaminants into soil and groundwater systems can greatly affect the quality of groundwater. A laboratory-designed large soil tank with periodic and continuous infiltration models, respectiv... The infiltration of water contaminants into soil and groundwater systems can greatly affect the quality of groundwater. A laboratory-designed large soil tank with periodic and continuous infiltration models, respectively, was used to simulate the migration of the contaminants NH4 and NO3 in a soil and groundwater system, including unsaturated and saturated zones. The unsaturated soil zone had a significant effect on removing NH4 and NO3 infiltrated from the surface water. The patterns of breakthrough curves of NH4 and NO3 in the unsaturated zone were related to the infiltration time. A short infiltration time resulted in a single sharp peak in the breakthrough curve, while a long infiltration time led to a plateau curve. When NH4 and NO3 migrated from the unsaturated zone to the saturated zone, an interracial retardation was formed, resulting in an increased contaminant concentration on the interface. Under the influence of horizontal groundwater movement, the infiltrated contaminants formed a contamination-prone area downstream. As the contaminants migrated downstream, their concentrations were significantly reduced. Under the same infiltration concentration, the concentration of NO3 was greater than that of NH4 at every corresponding cross-section in the soil and groundwater tank, suggesting that the removal efficiency of NH4 was greater than that of NO3 in the soil and groundwater system. 展开更多
关键词 breakthrough curve migration NH4 NO3 soil tank experiment
下载PDF
circMAN1A2调节miR-212-3p/DDIT4轴对胃癌细胞增殖、侵袭和迁移的影响
5
作者 曹博威 贾腾飞 +2 位作者 宋钉町 赵昱清 张文斌 《胃肠病学和肝病学杂志》 CAS 2024年第7期868-874,共7页
目的探究circMAN1A2靶向miR-212-3p/DNA损伤诱导转录子4(NDA damage-inducible transcript 4,DDIT4)轴对胃癌细胞增殖、侵袭和迁移的影响。方法qRT-PCR法检测胃癌组织和细胞中circMAN1A2、miR-212-3p表达水平。荧光素酶检测circMAN1A2与... 目的探究circMAN1A2靶向miR-212-3p/DNA损伤诱导转录子4(NDA damage-inducible transcript 4,DDIT4)轴对胃癌细胞增殖、侵袭和迁移的影响。方法qRT-PCR法检测胃癌组织和细胞中circMAN1A2、miR-212-3p表达水平。荧光素酶检测circMAN1A2与miR-212-3p、DDIT4和miR-212-3p的靶向关系。在胃癌细胞SGC-7901、HGC-27中转染si-NC、si-circMAN1A2、si-circMAN1A2+anti-NC、si-circMAN1A2+anti-miR-212-3p、miR-NC、miR-212-3p mimics,将未转染的SGC-7901、HGC-27细胞设为对照。平板克隆实验检测细胞增殖;细胞划痕及Transwell实验分别检测细胞迁移、侵袭能力。Western blotting检测增殖、迁移及侵袭相关蛋白表达。结果在胃癌组织及细胞中,circMAN1A2高表达,miR-212-3p低表达;下调circMAN1A2可以靶向上调miR-212-3p表达,且下调DDIT4表达,进而抑制胃癌细胞增殖、侵袭和迁移能力。抑制miR-212-3p表达可部分逆转抑制circMAN1A2表达对胃癌细胞恶性增殖的抑制作用。结论在胃癌细胞中抑制circMAN1A2表达可抑制胃癌细胞增殖、迁移与侵袭,其与调节miR-212-3p/DDIT4信号轴有关。 展开更多
关键词 环状RNA MAN1A2 微小RNA-212-3p DNA损伤诱导转录子4 胃癌 增殖 侵袭 迁移
下载PDF
固态电解质Li_(1+x)Al_(x)Ti_(2-x)(PO_(4))_(3)中Li+的迁移特性
6
作者 李梅 钟淑英 +2 位作者 胡军平 孙宝珍 徐波 《物理学报》 SCIE EI CAS CSCD 北大核心 2024年第13期356-366,共11页
Li_(1+x)Al_(x)Ti_(2-x)(PO_(4))_(3)(LATP)是一种颇具前景的NASICON型锂离子固态电解质.本文通过第一性原理计算研究了不同Al掺杂浓度(x=0.00,0.16,0.33,0.50)对LATP的结构特性、电学特性以及Li^(+)迁移特性的影响.结果表明,Al能够稳... Li_(1+x)Al_(x)Ti_(2-x)(PO_(4))_(3)(LATP)是一种颇具前景的NASICON型锂离子固态电解质.本文通过第一性原理计算研究了不同Al掺杂浓度(x=0.00,0.16,0.33,0.50)对LATP的结构特性、电学特性以及Li^(+)迁移特性的影响.结果表明,Al能够稳定掺杂进入LiTi2(PO4)3(LTP)的晶体结构当中.当Al掺杂浓度x=0.16时,Li—O键的平均键长最长,成键强度最弱,而Ti—O键强度随Al掺杂浓度变化不大.Al掺杂浓度对LATP带隙的影响不大,但Al附近的O原子聚集了更多的负电荷,形成AlO6极化中心.Li^(+)不同的迁移方式(空位迁移、间隙位迁移和协同迁移)在Al掺杂浓度不同时展现出复杂的能垒变化,Li^(+)在空位迁移中迁移势垒随Al掺杂浓度的增大而升高,而在间隙位迁移中Li^(+)的迁移势垒变化相反,由于协同迁移中涉及空位和间隙位两种位点,Li^(+)的迁移势垒表现为随Al掺杂浓度的升高先降低后升高的复杂变化.当x=0.50时,LATP具有最低的Li^(+)迁移势垒0.342 eV,这个势垒值是间隙位迁移的结果.因此,通过改变Al掺杂浓度,可改变间隙Li^(+)浓度及迁移通道结构,进而调节Li^(+)的迁移性能,提高LATP中的Li^(+)导电性能. 展开更多
关键词 全固态Li^(+)电池 AL掺杂 Li_(1+x)Al_(x)Ti_(2-x)(PO_(4))_(3) Li^(+)迁移
下载PDF
ANGPTL4通过调节上皮间充质转化促进舌癌细胞转移的分子机制研究
7
作者 董雨晴 张淑宁 +1 位作者 郭维华 张壮 《口腔生物医学》 2024年第1期32-37,共6页
目的:探究血管生成素样蛋白4(ANGPTL4)在舌癌进展及淋巴结转移中的分子机制,以期为舌癌的治疗提供新的分子靶点。方法:使用小干扰RNA(siRNA)沉默Tca8113细胞中的ANGPTL4基因,实时荧光定量PCR检验转染效率,通过CCK-8、Transwell和划痕实... 目的:探究血管生成素样蛋白4(ANGPTL4)在舌癌进展及淋巴结转移中的分子机制,以期为舌癌的治疗提供新的分子靶点。方法:使用小干扰RNA(siRNA)沉默Tca8113细胞中的ANGPTL4基因,实时荧光定量PCR检验转染效率,通过CCK-8、Transwell和划痕实验确定ANGPTL4沉默后Tca8113细胞的生物学行为变化;实时荧光定量PCR和Western blot实验检测细胞上皮间充质转化(EMT)相关指标的表达变化。结果:与空白对照组相比,siRNA沉默ANGPTL4后,细胞的增殖显著降低(P<0.01),且细胞迁移能力明显减弱(P<0.05)。与EMT相关的钙黏蛋白(E-cadherin)上调,波形蛋白(Vimentin)、盘装结构域受体1(DDR1)、锌指结合蛋白(ZEB-1)的表达下调。结论:ANGPTL4可以降低Tca8113细胞间黏附,促进Tca8113细胞的迁移和EMT,ANGPTL4可为舌癌淋巴结转移的潜在靶点。 展开更多
关键词 血管生成素样蛋白4 舌癌 增殖 侵袭 淋巴结转移
下载PDF
Inhibition of bromodomain-containing protein 4 enhances the migration of esophageal squamous cell carcinoma cells by inducing cell autophagy 被引量:1
8
作者 Wen-Qian Yang Rui Liang +3 位作者 Man-Qi Gao Yu-Zhen Liu Bo Qi Bao-Sheng Zhao 《World Journal of Gastrointestinal Oncology》 SCIE 2022年第12期2340-2352,共13页
BACKGROUND Esophageal squamous cell carcinoma(ESCC),the predominant type of esophageal cancer,has a 5-year survival rate less than 20%.Although the cause of poor prognosis is the high incidence and mortality of ESCC,t... BACKGROUND Esophageal squamous cell carcinoma(ESCC),the predominant type of esophageal cancer,has a 5-year survival rate less than 20%.Although the cause of poor prognosis is the high incidence and mortality of ESCC,the high rate of metastasis after esophageal cancer surgery is the main cause of death after the surgery.Bromodomain-containing protein 4(BRD4),an epigenetic reader of chromatinacetylated histones in tumorigenesis and development,plays an essential role in regulating oncogene expression.BRD4 inhibition and BRD4 inhibition-based treatment can potentially suppress ESCC growth.However,the effects and mechanisms of action of BRD4 on ESCC cell migration remain unclear.AIM To explore the effect of BRD4 on cell migration of ESCC in vitro and its possible molecular mechanism.METHODS Human ESCC cell lines KYSE-450 and KYSE-150 were used.The 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay was performed to examine cell proliferation,and the transwell migration assay was conducted to test ESCC cell migration.JQ1,a BRD4 inhibitor,was applied to cells,and BRD4 siRNA was transfected into ESCC cells to knockdown endogenous BRD4.GFP-RFP-LC3 adenovirus was infected into ESCC cells to evaluate the effect of JQ1 on autophagy.Western blotting was performed to determine the protein levels of BRD4,E-cadherin,vimentin,AMP-activated protein kinase(AMPK),and p-AMPK.RESULTS BRD4 was either downregulated by small interfering RNA or pretreated with JQ1 in ESCC cells,leading to increased tumor migration in ESCC cells in a dose-and time-dependent manner.Inhibition of BRD4 not only significantly suppressed cell proliferation but also strongly increased cell migration by inducing epithelial-mesenchymal transition(EMT).The protein expression of vimentin was increased and E-cadherin decreased in a dose-dependent manner,subsequently promoting autophagy in KYSE-450 and KYSE-150 cells.Pretreatment with JQ1,a BRD4 inhibitor,inhibited BRD4-induced LC3-II activation and upregulated AMPK phosphorylation in a dosedependent manner.Additionally,an increased number of autophagosomes and autolysosomes were observed in JQ1-treated ESCC cells.The autophagy inhibitor 3-methyladenine(3-MA)reversed the effects of BRD4 knockdown on ESCC cell migration and blocked JQ1-induced cell migration.3-MA also downregulated the expression of vimentin and upregulation E-cadherin.CONCLUSION BRD4 inhibition enhances cell migration by inducing EMT and autophagy in ESCC cells via the AMPK-modified pathway.Thus,the facilitating role on ESCC cell migration should be considered for BRD4 inhibitor clinical application to ESCC patients. 展开更多
关键词 JQ1 Bromodomain-containing protein 4 Cell migration Cell autophagy Epithelialmesenchymal transition Esophageal squamous cell carcinoma
下载PDF
SOX4通过靶向调节miR-17表达水平对结直肠癌细胞免疫逃逸及细胞迁移的影响
9
作者 王国强 张纲 +3 位作者 唐建坡 张玉国 杨永江 王俊新 《检验医学与临床》 CAS 2024年第13期1825-1830,1835,共7页
目的探究性别决定区Y框蛋白4(SOX4)通过靶向调节微小RNA(miR)-17表达水平对结直肠癌细胞免疫逃逸及细胞迁移的影响。方法采用实时荧光定量聚合酶链反应检测正常结直肠黏膜上皮细胞及4种结直肠癌细胞中SOX4、miR-17表达水平。取结直肠癌... 目的探究性别决定区Y框蛋白4(SOX4)通过靶向调节微小RNA(miR)-17表达水平对结直肠癌细胞免疫逃逸及细胞迁移的影响。方法采用实时荧光定量聚合酶链反应检测正常结直肠黏膜上皮细胞及4种结直肠癌细胞中SOX4、miR-17表达水平。取结直肠癌细胞将其分为结直肠癌细胞(CC)组、结直肠癌细胞+SOX4-NC(SN)组、结直肠癌细胞+SOX4激动剂(SM)组、结直肠癌细胞+SOX4抑制剂(SI)组、结直肠癌细胞+miR-17-NC(MN)组、结直肠癌细胞+miR-17激动剂(MM)组、结直肠癌细胞+miR-17抑制剂(MI)组、结直肠癌细胞+SOX4抑制剂+miR-17抑制剂(II)组。采用免疫印迹法检测程序性死亡受体-1(PD-1)及PD-1配体(PD-L1)表达水平,小室法检测细胞迁移数量,双荧光素酶报告基因检测各组细胞荧光素酶活性。结果4种结直肠癌细胞中SOX4、miR-17 mRNA表达水平明显高于FHC正常结直肠黏膜上皮细胞,差异均有统计学意义(P<0.05)。CC组与SN组PD-1、PD-L1蛋白表达水平及细胞迁移数量比较,差异均无统计学意义(P>0.05)。SM组PD-1、PD-L1蛋白表达水平及细胞迁移数量均明显高于SN组,SI组PD-1、PD-L1蛋白表达水平及细胞迁移数量均明显低于SM组,差异均有统计学意义(P<0.05)。CC组与MN组PD-1、PD-L1蛋白表达水平及细胞迁移数量比较,差异均无统计学意义(P>0.05)。MM组PD-1、PD-L1蛋白表达水平及细胞迁移数量均明显高于MN组,MI组PD-1、PD-L1蛋白表达水平及细胞迁移数量均明显低于MM组,差异均有统计学意义(P<0.05)。SI组与MI组PD-1、PD-L1蛋白表达水平及细胞迁移数量比较,差异均无统计学意义(P>0.05)。II组PD-1、PD-L1蛋白表达水平及细胞迁移数量均明显低于MI组,差异均有统计学意义(P<0.05)。双荧光素酶报告基因检测结果显示,转染SOX4后miR-17-3′-UTR-WT的荧光素酶活性明显升高,差异有统计学意义(P<0.05),miR-17-3′-UTR-MUT的荧光酶活性无明显变化,差异无统计学意义(P>0.05)。结论抑制SOX4表达水平可有效抑制结直肠癌细胞免疫逃逸,并抑制细胞迁移,其作用机制可能与抑制miR-17表达水平有关。 展开更多
关键词 性别决定区Y框蛋白4 微小RNA-17 结直肠癌 免疫逃逸 细胞迁移
下载PDF
A Model for Predicting Migration from IPV4 to IPV6 by 2027 in Nigeria 被引量:1
10
作者 Emmanuel Ekwonwune Nwabueze Ejike Nwosu C.   Oliver Eberechi Osuagwu 《Open Journal of Modelling and Simulation》 2018年第3期45-57,共13页
The present internet version which was established and consolidated over internet protocol version 4 (IPV4) in 1981, and whose amount of public addresses available is insufficient to meet the demands explosion and cur... The present internet version which was established and consolidated over internet protocol version 4 (IPV4) in 1981, and whose amount of public addresses available is insufficient to meet the demands explosion and current internet multimedia devices, services and application intensive environment has posed serious problems of incomplete web transactions. Stakeholders and communication industry in Nigeria are unwilling and feel reluctant to migrate to IPV6 because of inhibiting factors. This needs urgent redress to overcome the tractions that are responsible for apathy to migration from IPV4 to IPV6 launched in 1994 by the Internet Engineering Task Force (IETF). If nothing is done, sometime, internet may run out of space, ARIN [1]. Users may suffer disillusionment and frustration. The objective of this study therefore is to design a model for predicting migration from IPV4 to IPV6 in Nigeria by 2027 based on growth trend developed from statistical indices. The essence is to explore and analyze the factors that can encourage migration to IPV6 in the next 10 years and use those factors to forecast growth, so that IPV6 will receive boost in terms of growth and patronage. The study also aims at designing a predictive model that simulates the behaviour of the restrictive policies on migration to 1PV6 so as to ascertain the current impact on non-motivation and unwillingness to migrate to IPV6 in Nigeria. The motivation behind this study is to identify the inhibiting factors responsible for lack of motivation to migrate from IPV4 to IPV6 in Nigeria. The methodologies that were deployed in packaging the model include the statistical methodology, Structured Systems Analysis and Design Methodology (SSADM) and prototyping. The result is indeed functional software, programmed through Visual Basic. Net. (VB.Net) that can be used to simulate the behavioural impact of any government policy formulation for Telecommunication industry and stakeholders. 展开更多
关键词 MODEL Predicting migration IPV4 IPV6 INHIBITING Factors
下载PDF
miR-193b-3p过表达的HCT116外泌体对HUVEC增殖凋亡、迁移、血管形成影响及其与PAK4靶向关系
11
作者 孙玮螺 刘素英 +2 位作者 李思锦 周龙妹 何培元 《山东医药》 CAS 2024年第24期13-18,共6页
目的观察微小核糖核酸193b-3p(miR-193b-3p)过表达的人结直肠癌(CRC)细胞(HCT116)外泌体对人脐静脉内皮细胞(HUVEC)增殖凋亡、迁移、血管形成影响,并分析miR-193b-3p与p21活化蛋白激酶4(PAK4)的靶向关系。方法收集CRC患者血清和HCT116... 目的观察微小核糖核酸193b-3p(miR-193b-3p)过表达的人结直肠癌(CRC)细胞(HCT116)外泌体对人脐静脉内皮细胞(HUVEC)增殖凋亡、迁移、血管形成影响,并分析miR-193b-3p与p21活化蛋白激酶4(PAK4)的靶向关系。方法收集CRC患者血清和HCT116细胞上清外泌体,透射电镜实验和纳米颗粒示踪分析观察和鉴定外泌体,RT-q PCR实验检测外泌体miR-193b-3p和PAK4 m RNA。取人脐静脉内皮细胞(HUVEC),并分组,PBS组加入100μL的PBS,HCT116-Exo组加入100μL的HCT116细胞外泌体,HCT116-Exo+GW4869组先用GW4869(10μmol/L)处理30 min,然后加入100μL的HCT116细胞外泌体,采用Ed U实验、Transwell实验和成管实验检测各组HUVEC细胞增殖、迁移和血管形成能力。取对数生长期的HUVEC细胞,并分为miR-NC组、miR-193b-3p组,miR-NC组与转染miRNA阴性对照(miR-NC)的HCT116细胞外泌体共培养,miR-193b-3p组与转染miR-193b-3p模拟物(miR-193b-3p mimics)的HCT116细胞外泌体共培养,采用CCK8实验、流式细胞术实验和成管实验检测各组HUVEC细胞活性、细胞周期、细胞凋亡和血管形成能力。双荧光素酶报告基因系统检测miR-193b-3p和PAK4的靶向关系。结果CRC患者血清和细胞外泌体miR-193b-3p表达升高,PAK4 m RNA表达降低(P均<0.05);CRC细胞外泌体可促进HUVEC细胞的增殖、迁移和血管形成(P均<0.05);过表达CRC细胞外泌体miR-193b-3p增加HUVEC细胞活力和血管形成、加速细胞周期进程、抑制细胞凋亡(P均<0.05);miR-193b-3p直接靶向PAK4抑制其荧光素酶活性(P<0.05)。结论CRC血清、癌细胞外泌体miR-193b-3p表达升高,加入HCT116细胞外泌体的HUVEC细胞增殖、迁移和血管形成能力增强,加入转染miR-193b-3p mimics HCT116细胞外泌体的HUVEC细胞增殖、S期占比、血管形成能力升高及G_(0)/G_(1)期占比、凋亡率下降,miR-193b-3p与PAK4存在靶向关系。 展开更多
关键词 结直肠癌 外泌体 微小核糖核酸193b-3p P21活化蛋白激酶4 细胞增殖 细胞迁移 细胞凋亡 细胞周期 血管生成
下载PDF
过氧化物酶体膜蛋白4通过细胞外信号调节激酶1/2信号通路促进肝细胞癌细胞的上皮间质转化
12
作者 李巍 徐梓山 +3 位作者 马柯 张静雨 胡晓云 贺国洋 《中国肿瘤生物治疗杂志》 CAS CSCD 北大核心 2024年第8期786-795,共10页
目的:探讨过氧化物酶体膜蛋白4(PXMP4)对肝细胞癌(HCC)细胞迁移和侵袭及上皮间质转化(EMT)进程的影响。方法:采用生物信息学和免疫组织化学方法分析HCC组织中PXMP4的表达,分析其与患者临床病理特征的相关性。在HCCLM3和MHCC97H细胞中干... 目的:探讨过氧化物酶体膜蛋白4(PXMP4)对肝细胞癌(HCC)细胞迁移和侵袭及上皮间质转化(EMT)进程的影响。方法:采用生物信息学和免疫组织化学方法分析HCC组织中PXMP4的表达,分析其与患者临床病理特征的相关性。在HCCLM3和MHCC97H细胞中干扰PXMP4,在Huh7和MHCC97L细胞中过表达PXMP4,利用WB和qPCR法验证干扰/过表达效率。利用CCK-8、划痕愈合实验和Transwell侵袭实验检测干扰/过表达PXMP4对HCC细胞增殖、迁移和侵袭能力的影响,采用WB法检测干扰/过表达PXMP4或0、5、10和20μmol/L U0126处理对HCC细胞中N-cadherin、E-cadherin、vimentin、细胞外信号调节激酶(ERK)、p-ERK表达的影响。结果:生物信息学和免疫组织化学分析显示,HCC组织中PXMP4呈高表达(P<0.05)。临床病理分析发现,PXMP4的表达与肿瘤分化程度有关联(P<0.05)。在HCC细胞中,干扰PXMP4后抑制细胞增殖、侵袭和EMT进程(P<0.05);反之,过表达PXMP4后促进HCC细胞增殖、侵袭及EMT进程(P<0.05)。此外,PXMP4通过激活ERK1/2信号通路促进HCC细胞EMT进程,U0126处理同样能够抑制HCC细胞EMT进程。结论:PXMP4在HCC组织中呈高表达且与HCC细胞分化有关联,PXMP4通过激活ERK1/2信号通路促进HCC细胞EMT进程。 展开更多
关键词 肝细胞癌 过氧化物酶体膜蛋白4 细胞外信号调节激酶 迁移 侵袭 上皮间质转化
下载PDF
miR-193b-3p、PAK4过表达对人结肠癌细胞增殖凋亡和迁移侵袭的影响及靶向关系
13
作者 孙玮螺 刘素英 +2 位作者 李思锦 周龙妹 何培元 《山东医药》 CAS 2024年第12期1-5,共5页
目的观察微小核糖核酸193b-3p(miR-193b-3p)、P21活化蛋白激酶4(PAK4)过表达对人结肠癌细胞系HCT116细胞增殖凋亡和迁移侵袭的影响,并验证两者的靶向关系。方法体外培养人正常结肠黏膜上皮细胞FHC及人结肠癌细胞HCT116、SW480、LoVo,采... 目的观察微小核糖核酸193b-3p(miR-193b-3p)、P21活化蛋白激酶4(PAK4)过表达对人结肠癌细胞系HCT116细胞增殖凋亡和迁移侵袭的影响,并验证两者的靶向关系。方法体外培养人正常结肠黏膜上皮细胞FHC及人结肠癌细胞HCT116、SW480、LoVo,采用RT-PCR检测各细胞miR-193b-3p、P21活化蛋白激酶4(PAK4)mRNA。取生长状态良好的对数生长期HCT116细胞,分为4组,miR-NC组转染miRNA阴性对照、miR-193b-3p组转染miR-193b-3p模拟物、miR-193b-3p+PAK4-NC组转染miR-193b-3p模拟物+P21活化蛋白激酶4(PAK4)空载体、miR-193b-3p+PAK4组转染miR-193b-3p模拟物+PAK4过表达载体,分别采用RT-PCR、CCK-8试验、流式细胞术、Transwell实验检测各组细胞miR-193b-3p、PAK4 mRNA表达及增殖活性、凋亡率、迁移细胞数、侵袭细胞数。采用生物信息学软件Target Scan7.2预测miR-193b-3p与PAK4的靶向关系,并采用双荧光素酶报告基因实验进行验证。结果过表达miR-193b-3p后,HCT116细胞增殖活性、迁移及侵袭能力均明显下降,凋亡率明显升高,PAK4 mRNA表达水平降低(P均<0.05)。上调PAK4表达能够部分逆转过表达miR-193b-3p对HCT116细胞增殖活性、迁移及侵袭能力的抑制及对凋亡的促进作用(P均<0.05)。双荧光素酶报告基因显示miR-193b-3p能靶向结合PAK4的3'UTR区,抑制其荧光素酶活性(P<0.05)。结论miR-193b-3p过表达可抑制HCT116细胞增殖、迁移及侵袭,并促进其凋亡,miR-193b-3p与PAK4存在靶向关系。 展开更多
关键词 微小核糖核酸193b-3p 结肠癌 HCT116细胞 细胞增殖 细胞凋亡 细胞迁移 细胞侵袭 P21活化蛋白激酶4
下载PDF
Upregulation of stromal cell-derived factor-1 alpha/CXCR4 axis-induced migration of human neural progenitors by tumor necrosis factor-alpha and interleukin-8
14
作者 Jing Qu Hongtao Zhang +2 位作者 Guozhen Hui Xueguang Zhang Huanxiang Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2009年第11期832-837,共6页
BACKGROUND: Studies of several animal models of central nervous system diseases have shown that neural progenitor cells (NPCs) can migrate to injured tissues. Stromal cell-derived factor 1 alpha (SDF-la), and its... BACKGROUND: Studies of several animal models of central nervous system diseases have shown that neural progenitor cells (NPCs) can migrate to injured tissues. Stromal cell-derived factor 1 alpha (SDF-la), and its primary physiological receptor CXCR4, have been shown to contribute to this process. OBJECTIVE: To investigate migration efficacy of human NPCs toward a SDF-1α gradient, and the regulatory roles of tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8) in SDF-1α/CXCR4 axis-induced migration of NPCs. DESIGN, TIME AND SETTING: An in vitro, randomized, controlled, cellular and molecular biology study was performed at the Laboratory of Department of Cell Biology, Medical College of Soochow University between October 2005 and November 2007. MATERIALS: SDF-1α and mouse anti-human CXCR4 fusion antibody were purchased from R&D Systems, USA. TNF-αwas purchased from Biomyx Technology, USA and IL-8 was kindly provided by the Biotechnology Research Institute of Soochow University. METHODS: NPCs isolated from forebrain tissue of 9 to 10-week-old human fetuses were cultured in vitro. The cells were incubated with 0, 20, and 40 ng/mL TNF-α, or 0, 20, and 40 ng/mL IL-8, for 48 hours prior to migration assay. For antibody-blocking experiments, cells were further pretreated with 0, 20, and 40 μg/mL mouse anti-human CXCR4 fusion antibody for 2 hours. Subsequently, the transwell assay and CXCR4 blockade experiments were performed to evaluate migration of human NPCs toward a SDF-1α gradient. Serum-free culture medium without SDF-1α served as the negative control. MAIN OUTCOME MEASURES: The transwell assay was performed to evaluate migration of human NPCs toward a SDF-1α gradient, which was blocked by fusion antibody against CXCR4. In addition, CXCR4 expression in human NPCs stimulated by TNF-α and IL-8 was measured by flow cytometry. RESULTS: Results from the transwell assay demonstrated that SDF-1α was a strong chemoattractant for human NPCs (P 〈 0.01), and 20 ng/mL produced the highest levels of migration. Anti-human CXCR4 fusion antibody significantly blocked the chemotactic effect (P 〈 0.05). Flow cytometry results showed that treatment with TNF-α and IL-8 resulted in increased CXCR4 expression and greater chemotaxis efficiency of NPCs towards SDF-1α(P 〈 0.01). CONCLUSION: These results demonstrated that SDF-la significantly attracted NPCs in vitro, and neutralizing anti-CXCR4 antibody could block part of this chemotactic function. TNF-α and IL-8 increased chemotaxis efficiency of NPCs towards the SDF-1αgradient by upregulating CXCR4 expression in NPCs. 展开更多
关键词 human neural progenitor cells migration stromal cell-derived factor 1 alpha CXCR4 tumor necrosis factor-α INTERLEUKIN-8
下载PDF
含孤立四面体基元的AMO_(4)型质子导体的研究进展
15
作者 耿鑫悦 杭高庆 +1 位作者 欧长良 杨小燕 《材料导报》 EI CAS CSCD 北大核心 2024年第22期100-106,共7页
AMO_(4)(A=稀土元素,M=Nb,P,As,V…)氧化物因结构中含有灵活旋转和易变形的孤立MO 4四面体结构基元,有利于氧和质子的稳定和离子的长程迁移,是良好的无机固态离子导体候选体系。根据载流子种类可将无机固态离子导体主要分为氧离子导体... AMO_(4)(A=稀土元素,M=Nb,P,As,V…)氧化物因结构中含有灵活旋转和易变形的孤立MO 4四面体结构基元,有利于氧和质子的稳定和离子的长程迁移,是良好的无机固态离子导体候选体系。根据载流子种类可将无机固态离子导体主要分为氧离子导体和质子导体,与氧离子导体相比,质子导体具有较低的迁移能垒。本文首先概述了AMO_(4)型质子导体的晶体结构、导电性与受体掺杂剂对质子导电性的影响,以及部分结构中质子缺陷的稳定形式与离子迁移机制;然后总结了影响AMO_(4)型质子导体导电性、质子稳定及迁移的关键因素,包括A位和M位阳离子尺寸、MO 4四面体的畸变程度和相邻MO 4四面体氧离子之间的距离等;最后展望了AMO_(4)型质子导体未来的发展方向。 展开更多
关键词 AMO 4型质子导体 孤立四面体 缺陷稳定 离子迁移机制 构效关系
下载PDF
NRG4基因对胶质瘤细胞的增殖、迁移及侵袭的影响
16
作者 舒波 出良钊 +3 位作者 甘鸿川 黎浪 张胜 赵进城 《贵州医科大学学报》 CAS 2024年第4期508-514,共7页
目的探讨神经调节蛋白4(NRG4)对神经胶质瘤细胞的增殖、迁移以及侵袭作用的影响及机制。方法采用逆转录-定量聚合酶链反应(RT-qPCR)法检测神经胶质瘤患者(研究组)、对照组(同期健康志愿者)血清以及星形胶质细胞HA、神经胶质瘤细胞系U251... 目的探讨神经调节蛋白4(NRG4)对神经胶质瘤细胞的增殖、迁移以及侵袭作用的影响及机制。方法采用逆转录-定量聚合酶链反应(RT-qPCR)法检测神经胶质瘤患者(研究组)、对照组(同期健康志愿者)血清以及星形胶质细胞HA、神经胶质瘤细胞系U251、SHG44、LN229及T98G中NRG4和人表皮生长因子受体4(ErbB4)mRNA表达水平;将U251细胞分为Control组(空白对照)、NC组(转染不带RNA的质粒)、si-NRG4组(转染si-NRG4)和si-NRG4+ErbB4组[转染si-NRG4和ErbB4过表达质粒(pcDNA-ErbB4)]4组,通过细胞计数试剂盒-8(CCK-8)检测细胞增殖情况,划痕愈合实验和Transwell实验分析U251细胞的迁移与侵袭能力变化,免疫印迹(Western blot)检测PI3K/AKT通路中关键蛋白磷脂酰肌醇-3-激酶(PI3K)中p110α、p110β亚型、磷酸化丝氨酸/苏氨酸蛋白激酶(pAKT)中ser473和thr308 a以及蛋白激酶(AKT)表达水平。结果研究组血清中NRG4和ErbB4 mRNA表达量明显高于对照组(P<0.0001),神经胶质瘤细胞系U251中NRG4和ErbB4 mRNA相对表达量最高;与NC组比较,si-NRG4组中NRG4基因表达下调,不仅抑制U251细胞的增殖、迁移与侵袭,还降低了PI3 K-p110α,pAKT-ser473 and pAKT-thr308蛋白表达(P<0.05)。结论抑制NRG4表达可以减缓磷脂酰肌醇有关的信号通路PI3K/AKT通路的激活,抑制U251细胞的增殖和迁移,促进U251细胞凋亡,因此NRG4有可能成为治疗胶质瘤的潜在靶点。 展开更多
关键词 NRG4 ERBB4 PI3K/AKT 神经胶质瘤细胞 增殖 迁移 侵袭
下载PDF
环状RNA_PLEKHM3通过miR-320/KLF4轴调控宫颈癌细胞上皮间质转化
17
作者 张亚男 崔莹 +1 位作者 王天娇 杜忠蕾 《安徽医科大学学报》 CAS 北大核心 2024年第3期403-412,共10页
目的探讨环状RNA含普列克底物蛋白同源域的家族M3成员(PLEKHM3)(circRNA_PLEKHM3)通过调控微小RNA-320(miR-320)/畸变样因子4(KLF4)轴在宫颈癌细胞上皮间质转化(EMT)行为中的作用与机制。方法采用实时定量PCR(qRT-PCR)法检测宫颈癌细胞H... 目的探讨环状RNA含普列克底物蛋白同源域的家族M3成员(PLEKHM3)(circRNA_PLEKHM3)通过调控微小RNA-320(miR-320)/畸变样因子4(KLF4)轴在宫颈癌细胞上皮间质转化(EMT)行为中的作用与机制。方法采用实时定量PCR(qRT-PCR)法检测宫颈癌细胞Hela和CaSki中circRNA_PLEKHM3的表达水平;RNA荧光原位杂交检测circRNA_PLEKHM3在人宫颈癌上皮细胞CaSki中的定位;双荧光素酶报告基因实验检测circRNA_PLEKHM3和miR-320的靶向关系,以及miR-320和KLF4的靶向关系;对CaSki细胞过表达circRNA_PLEKHM3;另外设置三组,分别为在过表达circRNA_PLEKHM3的基础上过表达miR-320、沉默KLF4,以及在过表达miR-320的基础上沉默KLF4。qRT-PCR检测CaSki中miR-320的表达水平;Western blot检测CaSki细胞中KLF4和EMT标志物上皮钙黏蛋白(E-cadherin)、神经钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)、基质金属蛋白酶(MMP)-2和MMP-9的表达;Transwell实验检测细胞迁移数和侵袭细胞数。结果circRNA_PLEKHM3在Hela和CaSki中的表达均降低(P<0.05),其主要定位在细胞质中;双荧光素酶报告基因实验显示miR-320和circRNA_PLEKHM3存在靶向关系,KLF4和miR-320存在靶向关系;过表达circRNA_PLEKHM3抑制miR-320和N-cadherin、Vimentin、MMP-2、MMP-9的蛋白表达,上调E-cadherin的蛋白表达,减少细胞迁移和侵袭数(P<0.05);在过表达circRNA_PLEKHM3的基础上过表达miR-320或沉默KLF4均能够促进miR-320和N-cadherin、Vimentin、MMP-2、MMP-9蛋白的表达,上调E-cadherin蛋白的表达,减少迁移和侵袭细胞数(P<0.05);然而在过表达miR-320的基础上沉默KLF4,KLF4和N-cadherin、Vimentin、MMP-2、MMP-9蛋白的表达受到抑制,E-cadherin蛋白的表达上调,细胞迁移和侵袭数减少(P<0.05)。结论circRNA_PLEKHM3过表达可能通过miR-320/KLF4轴调控宫颈癌细胞的EMT。 展开更多
关键词 cirRNA_PLEKHM3 miRNA-320 畸变样因子4 宫颈癌细胞 上皮间质转化 迁移 侵袭
下载PDF
Correlation of KLF4 and UBE2C expression levels in neuroblastoma with cell adhesion and migration
18
作者 Tao Zhang Hui-Lin Mao Li Feng 《Journal of Hainan Medical University》 2017年第23期80-83,共4页
Objective: To study the correlation of KLF4 and UBE2C expression levels in neuroblastoma with cell adhesion and migration. Methods: A total of 56 children who were diagnosed with neuroblastoma in the Central Hospital ... Objective: To study the correlation of KLF4 and UBE2C expression levels in neuroblastoma with cell adhesion and migration. Methods: A total of 56 children who were diagnosed with neuroblastoma in the Central Hospital of Enshi Autonomous Prefecture between May 2014 and February 2017 were selected as the NB group of the study, and the lesion tissue was collected;38 children who were treated in the Central Hospital of Enshi Autonomous Prefecture due to serious hydronephrosis during the same period were selected as the control group of the study, and the normal adrenal gland tissue was collected. The mRNA expression and protein expression of KLF4 and UBE2C as well as the protein expression of cell adhesion molecules and migration molecules in clinical tissue samples were determined. Results: The mRNA expression and protein expression of KLF4 in neuroblastoma tissue of NB group were greatly lower than those of control group whereas the mRNA expression and protein expression of UBE2C were greatly higher than those of control group;PDLIM1, AMF, GPx1, L1CAM, Nrg1, RANK, RANKL, Inβ1, MTA1 and MMP9 protein expression in neuroblastoma tissue of NB group were greatly higher than those of control group, negatively correlated with the protein expression KLF4, and positively correlated with the protein expression of UBE2C. Conclusion: The low expression of KLF4 and the high expression of UBE2C in neuroblastoma can promote the adhesion and migration of tumor cells. 展开更多
关键词 NEUROBLASTOMA Kruppel-like factor 4 Ubiquitin-conjugating ENZYME 2C Adhesion migration
下载PDF
双氢青蒿素抑制TLR4/NF-κB信号通路对高糖刺激的足细胞功能障碍的改善作用 被引量:1
19
作者 张云 陈小青 +2 位作者 李月婷 施书涵 林长达 《中药新药与临床药理》 CAS CSCD 北大核心 2023年第8期1075-1082,共8页
目的探究双氢青蒿素通过调控Toll样受体4(TLR4)/核因子-κB(NF-κB)信号通路对D-葡萄糖诱导的人肾小球足细胞(HGPC)炎症、增殖、迁移和侵袭的影响。方法体外培养HGPC细胞,将HGPC细胞分为对照组(5 mmol·L^(-1)D-葡萄糖)、高糖组(30 ... 目的探究双氢青蒿素通过调控Toll样受体4(TLR4)/核因子-κB(NF-κB)信号通路对D-葡萄糖诱导的人肾小球足细胞(HGPC)炎症、增殖、迁移和侵袭的影响。方法体外培养HGPC细胞,将HGPC细胞分为对照组(5 mmol·L^(-1)D-葡萄糖)、高糖组(30 mmol·L^(-1)D-葡萄糖)和不同浓度双氢青蒿素组(30 mmol·L^(-1)D-葡萄糖+5、10、20、40μmol·L^(-1)双氢青蒿素),筛选出合适的双氢青蒿素作用浓度;随后将细胞分为对照组、高糖组、双氢青蒿素组(30 mmol·L^(-1)D-葡萄糖+20μmol·L^(-1)双氢青蒿素)、抑制剂组(30 mmol·L^(-1)D-葡萄糖+5μmol·L^(-1)NF-κB通路抑制剂BAY 11-7082)、双氢青蒿素+抑制剂组(30 mmol·L^(-1)D-葡萄糖+20μmol·L^(-1)双氢青蒿素+5μmol·L^(-1)BAY 11-7082)和双氢青蒿素+激活剂组(30 mmol·L^(-1)D-葡萄糖+20μmol·L^(-1)双氢青蒿素+1μmol·L^(-1)NF-κB通路激活剂Prostratin),干预24 h。细胞计数试剂盒细胞8(CCK-8)法检测细胞活力;酶联免疫吸附试验(ELISA)法检测炎症因子白细胞介素(IL)-1β和IL-8的表达水平;5-乙炔基-2’脱氧尿嘧啶核苷(EdU)法检测细胞的增殖能力;Transwell小室法检测细胞迁移和侵袭能力;蛋白免疫印迹(Western Blot)法检测细胞周期蛋白D1(CyclinD1)、基质金属蛋白酶9(MMP-9)和TLR4/NF-κB通路相关蛋白表达水平。结果CCK-8法检测结果显示20μmol·L^(-1)双氢青蒿素对D-葡萄糖HGPC细胞活力恢复效果最好,因此选择20μmol·L^(-1)双氢青蒿素用于后续实验。与对照组比较,高糖组细胞增殖率和CyclinD1蛋白相对表达量明显降低(P<0.05),炎症因子(IL-1β和IL-8)、迁移数、侵袭数、MMP-9、TLR4和磷酸化(p)-NF-κB p65蛋白相对表达量明显升高(P<0.05);双氢青蒿素组、抑制剂组、双氢青蒿素+抑制剂组及双氢青蒿素+激活剂组中双氢青蒿素和BAY11-7082明显抑制了D-葡萄糖对HGPC细胞的上述作用(P<0.05);与双氢青蒿素组比较,双氢青蒿素+抑制剂组中BAY11-7082增强了双氢青蒿素对D-葡萄糖诱导的HGPC细胞的作用(P<0.05),双氢青蒿素+激活剂组中Prostratin则削弱了双氢青蒿素对D-葡萄糖诱导的HGPC细胞的作用(P<0.05)。结论双氢青蒿素能抑制D-葡萄糖诱导的HGPC细胞迁移和侵袭,并促进其增殖,能有效改善D-葡萄糖刺激对HGPC细胞的炎症损伤,其作用机制可能与阻滞TLR4/NF-κB信号通路信号转导有关。 展开更多
关键词 糖尿病肾病 人肾小球足细胞 D-葡萄糖 双氢青蒿素 Toll样受体4/核因子-κB信号通路(TLR4/NF-κB) 炎症 增殖 迁移 侵袭
下载PDF
Synthesis of 2-(N-formyl)-5-aryl/aryloxymethyl-1,3,4-thiadiazoles with potential bioactivity in PEG-400 被引量:1
20
作者 Wang, Xi Cun Ding, Xiao Mei +2 位作者 Wang, Sheng Qing Chen, Xue Fei Quan, Zheng Jun 《Chinese Chemical Letters》 SCIE CAS CSCD 2010年第3期301-304,共4页
An environmental benign procedure for synthesis of 2-(N-formyl)-5-aryl/aryloxymethyl-1,3,4-thiadiazoles has been developed by reaction of 2-amino-5-aryl/aryloxymethyl-1,3,4-thiadiazoles with formic acid in PEG-400.The... An environmental benign procedure for synthesis of 2-(N-formyl)-5-aryl/aryloxymethyl-1,3,4-thiadiazoles has been developed by reaction of 2-amino-5-aryl/aryloxymethyl-1,3,4-thiadiazoles with formic acid in PEG-400.The key advantages of this protocol are the shorter reaction time,higher yields,lower cost,simple workup,and environment-friendly compared to conventional organic solvent reaction.The present method does not involve any hazardous organic solvent or catalyst. 展开更多
关键词 2-(N-Formyl)-5-aryl/aryloxymethyl-1 3 4-thiadiazoles 2-Amino-5-aryl/aryloxymethyl-1 PEG-400 Synthesis
下载PDF
上一页 1 2 15 下一页 到第
使用帮助 返回顶部