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细胞显微荧光定量分析系统的设计与研制 被引量:2
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作者 范世福 张思祥 +3 位作者 肖松山 赵玉春 孙振东 李彦芳 《天津大学学报》 EI CAS CSCD 1999年第1期45-48,共4页
在普通荧光显微镜基础上,设计和研制了整套光电系统和计算机系统,实现了细胞显微荧光光谱分析和细胞内生物物质的定量检测目标,为开发新颖有效、符合我国国情的显微荧光分析仪器解决了理论和关键技术问题.
关键词 显微分析 显微荧光检测 细胞生化分析
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壳寡糖对过氧化氢诱导肝细胞损伤的改善作用及机制 被引量:1
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作者 刘朋 侯智兴 +6 位作者 茅洪维 李恒 龚劲松 蒋敏 许泓瑜 许正宏 史劲松 《食品科学》 EI CAS CSCD 北大核心 2023年第5期136-142,共7页
目的:评估壳寡糖(chitooligosaccharides,COS)对过氧化氢(H_(2)O_(2))诱导肝细胞损伤的改善作用。方法:通过H_(2)O_(2)建立L-02细胞氧化应激损伤模型,对活性氧(reactive oxygen species,ROS)、线粒体膜电位以及IL-6、TNF-α等病程相关... 目的:评估壳寡糖(chitooligosaccharides,COS)对过氧化氢(H_(2)O_(2))诱导肝细胞损伤的改善作用。方法:通过H_(2)O_(2)建立L-02细胞氧化应激损伤模型,对活性氧(reactive oxygen species,ROS)、线粒体膜电位以及IL-6、TNF-α等病程相关基因水平进行分析。结果:COS可改善H_(2)O_(2)损伤L-02细胞的增殖活力、抑制线粒体膜电位下降和ROS水平升高(P<0.05)。单细胞纳米生化分析结果显示,COS处理可以平衡H_(2)O_(2)损伤L-02细胞的ROS水平波动幅度。另外,COS改善了炎症(IL-6、TNF-α)、凋亡(Caspase 3、Caspase 9、Bax、Bcl-2)及氧化应激(Nrf2、HO-1)相关基因转录水平,表现出抗凋亡和抗氧化应激的作用。结论:COS对H_(2)O_(2)损伤的L-02细胞具有保护作用,本实验可为COS的应用开发提供理论参考。 展开更多
关键词 壳寡糖 氧化应激 细胞 细胞凋亡 细胞纳米生化分析
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Baicalin and geniposide inhibit the development of atherosclerosis by increasing Wntl and inhibiting dickkopf-related protein-1 expression 被引量:8
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作者 Bin WANG Ping-Ping LIAO +3 位作者 Li-Hua LIU Xin FANG Wei LI Si-Ming GUAN 《Journal of Geriatric Cardiology》 SCIE CAS CSCD 2016年第10期846-854,共9页
Background Our previous study showed that the combined Chinese herbs containing scutellaria baicalensis georgi and gardenia jasminoids ellis inhibited atherosclerosis. In this study, we sought to determine if baicalin... Background Our previous study showed that the combined Chinese herbs containing scutellaria baicalensis georgi and gardenia jasminoids ellis inhibited atherosclerosis. In this study, we sought to determine if baicalin and geniposide could inhibit atherosclerosis through Wntl and dickkopf-related protein-1 (DKK1). Methods The wild-type and ApoE-/- mice were treated with baicalin, geniposide, and baicalin plus geniposide daily by gavage for 12 weeks. Blood lipid levels were measured with an automatic biochemistry analyzer. Aortic atherosclerotic lesion areas were analyzed with Image-ProPlus software. The mRNA and protein expression of DKK1, Wntt and nuclear factor-r,B (NF-κB) were measured with RT-PCR and Westem Blot. Serum levels of interleukin-12 (IL-12) were quantified with ELISA. Results The baicalin or geniposide monotherapy as well as combination therapy inhibited the development of atherosclerotic lesions, increased Wntl and decreased DKKI expression and elevated the ratio of Wntl/DKK1 compared with high-lipid diet group. However, only baicalin or geniposide monotherapy decreased NF-κB expression. Moreover, baicalin and geniposide monoor combination therapy lowered IL-12 levels. Geniposide reduced both serum total cholesterol and low density lipoprotein levels, while baicalin either alone or in combination with geniposide did not affect serum lipid levels. In human, umbilical vein endothelial ceils stimulated by oxidized low density lipoprotein, baicalin and geniposide also increased Wntl and decreased DKK1 expression and elevated the ratio of Wntl/DKK1. Condusions Baicalin and geniposide exert inflammation-regulatory effects and may prevent atherosclerotic lesions through enhancing Wntl and inhibit- ing DKK1 expression. 展开更多
关键词 ATHEROSCLEROSIS BAICALIN DKK1 GENIPOSIDE Wntl
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System Size Resonance Associated with Canard Phenomenon in a Biological Cell System
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作者 Juan Ma Hong-ying Li +1 位作者 Zhong-huai Hou Hou-wen Xin 《Chinese Journal of Chemical Physics》 SCIE CAS CSCD 北大核心 2008年第6期521-525,共5页
The influence of internal noise on the calcium oscillations is studied. It is found that stochastic calcium oscillations occur when the internal noise is considered, while the corresponding deterministic dynamics only... The influence of internal noise on the calcium oscillations is studied. It is found that stochastic calcium oscillations occur when the internal noise is considered, while the corresponding deterministic dynamics only yields a steady state. Also,. the performance of such oscillations shows two maxima with the variation of the system size, indicating the occurrence of system size resonance. This behavior is found to be intimately connected with the canard phenomenon. Interestingly, it is also found that one of the optimal system sizes matches well with the real cell size, and such a match is robust to the variation of the control parameters. 展开更多
关键词 Internal noise Calcium oscillations System size resonance Canard phenomenon
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Aurora A orchestrates entosis by regulating a dynamic MCAK-TIP150 interaction 被引量:9
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作者 PengXia JinhuaZhou +13 位作者 Xiaoyu Song BingWu XingLiu Di Li Shuyuan Zhang Zhikai Wang H uijuan Yu Tarsha Ward Jiancun Zhang Yinmei Li Xiaoning Wang YongChen Zhen Guo Xuebiao Yao 《Journal of Molecular Cell Biology》 SCIE CAS CSCD 2014年第3期240-254,共15页
Entosis, a ceU-in-ceU process, has been implicated in the formation of aneuploidy associated with an aberrant cell division control. Microtubule plus-end-tracking protein TI P150 facilitates the loading of MCAK onto t... Entosis, a ceU-in-ceU process, has been implicated in the formation of aneuploidy associated with an aberrant cell division control. Microtubule plus-end-tracking protein TI P150 facilitates the loading of MCAK onto the microtubule plus ends and orchestrates micro- tubule plus-end dynamics during cell division. Here we show that TIP150 cooperates with MCAK to govern entosis via a regulatory cir- cuitry that involves Aurora A-mediated phosphorylation of MCAK. Our biochemical analyses show that MCAK forms an intra-molecular association, which is essential for TIP150 binding. Interestingly, Aurora A-mediated phosphorylation of MCAK modulates its intra-mo- lecular association, which perturbs the MCAK-TI P150 interaction in vitro and inhibits entosis in vivo. To probe if MCAK-TIP150 inter- action regulates microtubule plasticity to affect the mechanical properties of ceUs during entosis, we used an optical trap to measure the mechanical rigidity of live MCF7 ceils. We find that the MCAK cooperates with TIP150 to promote microtubule dynamics and modulate the mechanical rigidity of the cells during entosis. Our results show that a dynamic interaction of MCAK-TI P150 orchestrated by Aurora A-mediated phosphorylation governs entosis via regulating microtubule plus-end dynamics and cell rigidity. These data reveal a previously unknown mechanism of Aurora A regulation in the control of microtubule plasticity during ceU-in-ceU pro- cesses. 展开更多
关键词 Aurora A TIP150 MCAK entosis microtubule plus-end KINESIN
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Bidirectional effect of Wnt signaling antagonist DKK1 on the modulation of anthrax toxin uptake 被引量:2
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作者 QIAN LiLi CAI ChangZu +7 位作者 YUAN PengFei JEONG Sun-Young YANG XiaoZhou DEALMEIDA Venita ERNST James COSTA Michael COHEN Stanley N. WEI WenSheng 《Science China(Life Sciences)》 SCIE CAS 2014年第5期469-481,共13页
LRP6, a co-receptor for the morphogen Wnt, aids endocytosis of anthrax complexes. Here we report that Dickkopfl (DKK1) protein, a secreted LRP6 ligand and antagonist, is also a modulator of anthrax toxin sensitivity... LRP6, a co-receptor for the morphogen Wnt, aids endocytosis of anthrax complexes. Here we report that Dickkopfl (DKK1) protein, a secreted LRP6 ligand and antagonist, is also a modulator of anthrax toxin sensitivity, shRNA-mediated gene silencing or TALEN-mediated gene knockout of DKK1 reduced sensitivity of cells to PA-dependent hybrid toxins. However, unlike the solely inhibitory effect on Wnt signaling, the effects of DKK1 overexpression on anthrax toxicity were bidirectional, depending on its endogenous expression and cell context. Fluorescence microscopy and biochemical analyses showed that DKK1 facilitates internalization of anthrax toxins and their receptors, an event mediated by DKK1-LRP6-Kremen2 complex. Monoclonal antibodies against DKK1 provided dose-dependent protection to macrophages from killing by anthrax lethal toxin (LT). Our discovery that DKK1 forms ternary structure with LRP6 and Kremen2 in promoting PA-mediated toxin internalization provides a paradigm for bacterial exploitation of mechanisms that host cells use to internalize signaling proteins. 展开更多
关键词 DKK1 anthrax toxin LRP6 TALENs INTERNALIZATION Kremen2 receptor WNT
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