Kv1.3钾通道在ⅡA型分泌型磷脂酶A2诱导动脉粥样硬化形成过程中的作用－ 厦门大学学术典藏库－ Xiamen University Institutional Repository
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dc.contributor.advisor李庆阁
dc.contributor.author徐雪晶
dc.date.accessionedT03:22:05Z
dc.date.availableT03:22:05Z
dc.date.issued 16:42:15.0
dc.identifier.urihttp://dspace./handle/
dc.description.abstract研究背景和目的：IIA型分泌型磷脂酶A2（sPLA2-IIA）作为一类磷脂酶可通过其酶的催化作用和本身的致炎症作用而促进动脉粥样硬化（AS）的发生发展。Kv1.3钾通道活性增高与AS相关性疾病密切相关。二者均可通过调节树突状细胞（DCs）的分化与抗原递呈功能参与AS的发生发展，然而二者之间的相互关系如何尚待进一步阐明。本研究分别在细胞水平和组织水平上探讨Kv1.3钾通道在诱导动脉粥样硬化形成过程中的作用。 方法：1.在单核细胞分化为树突状细胞（DCs）的过程中，用不同浓度sPLA2-IIA干预，观察Kv1.3钾通道表达的变化；阻断Kv1.3钾通道对共刺激分子表达的影响。2.在树突状细胞分化为...
dc.description.abstractBackground & Objective: Group IIA Secretory Phospholipase A2 (sPLA2-IIA) aggravated atherosclerosis (AS) progress via itself catalysis and pro-inflammation. Upregulating Kv1.3 potassium channel activity was closely bound up with AS. Both sPLA2-IIA and Kv1.3 potassium channel regulated the differentiation and antigen-presenting function of dendritic cells (DCs), thus participating in the developmen...
dc.language.isozh_CN
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dc.source.urihttp://210.34.4.13:8080/lunwen/detail.asp?serial=43909
dc.subject动脉粥样硬化
dc.subjectIIA型分泌型磷脂酶A2
dc.subjectKv13钾通道
dc.subject树突状细胞
dc.subject血凝素样氧化低密度脂蛋白受体-1
dc.subjectAtherosclerosis
dc.subjectGroup IIA Secretory Phospholipase A2
dc.subjectKv13 Potassium Channel
dc.subjectDendrite Cells
dc.subjectLectin Like Oxidized Low Density Lipoprotein Receptor-1
dc.titleKv1.3钾通道在ⅡA型分泌型磷脂酶A2诱导动脉粥样硬化形成过程中的作用
dc.title.alternativeThe Effects of Kv1.3 Potassium Channel on Atherosclerosis Induced by Group IIA Secretory Phospholipase A2
dc.typethesis
dc.date.replied
dc.description.note学位：博士后
dc.description.note院系专业：生命科学学院_生物学
dc.description.note学号：
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Kv1.3钾通道在ⅡA型分泌型磷脂酶A2诱导动脉粥样硬化形成 ...
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(2) Subcloning pJC13-SR which has a promoter and a enhancer of human scavenger receptor A,a human growth hormone tail and
(2)利用pJC13(backbone：pGEM4Z)，构建带有染色质隔离子和清道夫受体A(scavenger receptor A，SR-A)增强子、启动子和人生长激素尾(hGH tail)的亚克隆pJC13-SR；
Changes of Scavenger Receptor Class B Type Ⅰ Expression in Mini Swine, HepG2 and THP-1 Cells
B类Ⅰ型清道夫受体在小型猪及HepG2、THP-1细胞中表达的变化
Effects of IL-10 on the expression of scavenger receptor and CD14 in murine alveolar macrophages
IL-10对小鼠肺泡巨噬细胞清道夫受体及CD14表达的影响
AMs were incubated
and stimulated with IL
10. The expressions of scavenger receptor (SR) and CD14 mRNA in AMs were observed with RT
方法　通过体外培养肺泡巨噬细胞 ,施加IL 6和IL 10刺激 ,应用RT PCR方法观察肺泡巨噬细胞CD14和清道夫受体 (SR)mRNA的表达变化。
The impact of scavenger receptor class A typeⅠ/Ⅱ on lipid metabolism in mice
清道夫受体AⅠ/Ⅱ对小鼠脂质代谢的影响
Objective To study the mRNA expression of hepatic scavenger receptor B type I(SRBI) and liver receptor homologue 1(LRH-1) in patients with cholesterol gallstone disease,and to elucidate the bio-molecular pathogenesis of gallstone formation.
目的:研究胆固醇结石病人BI型清除剂受体(scavengerreceptorBtypeI,SRBI)及其转录调节因子肝脏受体类似物1(liverreceptorhomologue1,LRH-1)的表达,以探讨胆固醇结石发病的机制。
Inhibition of Scavenger Receptor A Expression Treated with
PMA by the Inhibitor of Tyrosine Protein Kinase Genistein
酪氨酸蛋白激酶抑制剂genistein对PMA处理后A类清道夫受体表达的抑制
Advances in Class B Scavenger Receptor CD36
B类清道夫受体CD36的研究进展
The Truncation 1 to 27 Amino Acid Residues of the N-Terminal Cytoplasmic Domain Mediate the Function of Scavenger Receptor A
A类清道夫受体N端第1～27位氨基酸胞浆结构域缺失对功能的影响
A Therapeutic Target for Atherosclerosis:Scavenger Receptor A
治疗动脉粥样硬化的靶位:A类清道夫受体
The class A scavenger receptor (SR-A) is a glycoprotein expressed on the cell surface of macrophages that mediates internalization of chemically modified lipoprotein.
A类清道夫受体(Scavenger receptor，SR-A)是一种主要位于巨噬细胞膜表面的同源三聚体糖蛋白，能够介导多种配体进行内移。
Influences of wild-type p53 gene overexpression on the differentiation, apoptosis and expression of scavenger receptor CD36 in U937 cells
野生型p53基因导入对U937细胞分化、凋亡和CD36受体表达的影响(英文)
Effects of advanced glycation end products on expression of scavenger receptor class B type I (SR-BI) in U937 macrophages
糖基化终产物AGEs对U937巨噬细胞高密度脂蛋白受体(SR-BI)蛋白表达的影响(英文)
Aim: To investigate the roles of CD 14 and Scavenger receptor(SR) in the Bile Duct emphraxis-induced Hepatic injury, and the influence of glycine to CD14 and SR's expression.
目的：从受体水平上探讨CD14和SR在由胆道阻塞所致肠源性内毒素血症引发的“继发性肝损伤”中的作用，以及甘氨酸在防治这种“继发性肝损伤”中对CD14和SR表达的影响。
Objective:To study the role of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1),the specific scavenger receptor for oxidized low-density lipoprotein (ox-LDL),in the expression of transforming growth factor-β1 (TGF-β1) induced by ox-LDL in human glomerular mesangial cells.
目的:探讨血凝素样氧化低密度脂蛋白受体1(LOX-1)在氧化低密度脂蛋白(ox-LDL)诱导人肾小球系膜细胞(HGMC)表达转化生长因子(TGF-β1)中的作用。
Involvement of scavenger receptor A in suppression of RAW264.7 inflammatory cytokines release induced by LPS
SR-A受体参与抑制LPS刺激RAW264.7产生炎症因子
查询“scavenger receptor”译词为用户自定义的双语例句&&&&我想查看译文中含有：的双语例句
为了更好的帮助您理解掌握查询词或其译词在地道英语中的实际用法，我们为您准备了出自英文原文的大量英语例句，供您参考。&&&&&&&&&&&& It was found that the Lao Shan polsaccharide P, one of the chemical components of polystictus versicolor increased the number of acetylated low density lipoprotein ( acLDL ) receptorsin the macrophages and stimulated the binding, internalization and degradation of (125I ) acLDL by the macrophages in vitro. The effect on cell degradation of ( 125I ) acLDL was dose-effect. At 100μg/ ml of the Lao Shan polysaccharide P, the effect was maximum and the degradation of ( 125I ) acLDL increased 77% ( P<0.001 ) . These... It was found that the Lao Shan polsaccharide P, one of the chemical components of polystictus versicolor increased the number of acetylated low density lipoprotein ( acLDL ) receptorsin the macrophages and stimulated the binding, internalization and degradation of (125I ) acLDL by the macrophages in vitro. The effect on cell degradation of ( 125I ) acLDL was dose-effect. At 100μg/ ml of the Lao Shan polysaccharide P, the effect was maximum and the degradation of ( 125I ) acLDL increased 77% ( P<0.001 ) . These results suggested that the Lao Shan polysaccharide P might act as lipid-lowering and antiatherogenic drug in vivo through stimulating the scavenger receptor Pathway of macrophages.老山云芝多糖P可使小鼠腹腔巨噬细胞乙酰LDL(acLDL)受体数目增加。提高巨噬细胞对acLDL的结合、内移和降解。其对巨噬细胞降解acLDL的影响呈浓度效应关系,该效应在云芝多糖100μg/ml时最大,可使巨噬细胞对(~(125)Ⅰ)ac LDL的降解增加77%。实验结果提示,老山云芝多糖P可能通过刺激清道夫受体途径在整体发挥降脂、抗动脉粥样硬化的作用。 After oxidative modification by Cu2+ or by incubation with mouse peritoneal macrophages (MPM) or by irradiation with ultraviolet light (UV), lipoperoxidation and molecular structure variations in low density lipoproteins(LDL) were observed,as the thiobarbituric acid reactive substances (TBARS) , relative electrophoresis mobility (REM), fluorescence emission spectra and degradation rate by scavenger receptors were all increased markedly. We think that oxidative modification of LDL is probably an ideal model... After oxidative modification by Cu2+ or by incubation with mouse peritoneal macrophages (MPM) or by irradiation with ultraviolet light (UV), lipoperoxidation and molecular structure variations in low density lipoproteins(LDL) were observed,as the thiobarbituric acid reactive substances (TBARS) , relative electrophoresis mobility (REM), fluorescence emission spectra and degradation rate by scavenger receptors were all increased markedly. We think that oxidative modification of LDL is probably an ideal model for the study of lipoperoxidation, of the effect and the mechanism of antioxidant, as well as of the mechanism of atherogenesis.用Cu~(2+)诱导和小鼠腹腔巨噬细胞(MPM)共同孵育以及紫外线(UV)照射的方法都能够导致LDL的氧化修饰,表现在巴比妥酸反应物质(TBARS)、相对电泳迁移率(REM)、在420nm的荧光强度和经清道夫受体的降解速率等的增加。LDL的脂质过氧化修饰,除用作研究动脉粥样硬化的发生发展的机制外,还是一种研究脂质过氧化损伤和比较抗氧化剂的抗氧化效果及其作用机理的较为理想的模型。 Both oxidatively and malondialdehyde mosified low density lipoprotein (Ox—LDL and MDA—LDL)could be recongized by the scavenger receptor and induce intracellular cholesteryl ester accumulation of macrophage. The cholesteryl ester accumulation caused by MDA—LDL could be cleared by high density lipoprotein (HDL_3),but that caused by Ox—LDL could not be cleared. Further studies showed that both Ox—LDL and MDA—LDL could decrease the binding capacity of HDL_3 and increase the intracellular lipid peroxide (LPO).... Both oxidatively and malondialdehyde mosified low density lipoprotein (Ox—LDL and MDA—LDL)could be recongized by the scavenger receptor and induce intracellular cholesteryl ester accumulation of macrophage. The cholesteryl ester accumulation caused by MDA—LDL could be cleared by high density lipoprotein (HDL_3),but that caused by Ox—LDL could not be cleared. Further studies showed that both Ox—LDL and MDA—LDL could decrease the binding capacity of HDL_3 and increase the intracellular lipid peroxide (LPO). When macrophage was first cultured with MDA—LDL and then in medium containing 10% (v/v) lipoprotein deficent serum, the decreased binding capacity of HDL_3 was somewhat recovered and the intracellular LPO did not increase any more. However,if macrophage was first cultured with Ox—LDL,the binding capacity of HDL_3 continued to decrease and intracellular LPO continued to increase. There was negative correlation (r=-0.81, p<0.01) between the decrease of the binding capacity of HDL_3 and the increase of intracellular LPO caused by Ox—LDL. These results suggested that lipid peroxidative injury of Ox—LDL may play an important role in the transformation of macrophages to foam cells.氧化修饰低密度脂蛋白(Ox—LDL)在动脉粥样硬化发生发展中的作用越来越引起人们的重视。本文通过比较Ox—LDL和脂质过氧化降解产物丙二醛(MDA)修饰的低密度脂蛋白(MDA—LDL)在致泡沫细胞形成方面的差异,探讨了脂质过氧化对巨噬细胞的损伤在泡沫细胞形成中的作用。结果显示:Ox—LDL和MDA—LDL都可被巨噬细胞清道夫受体所识别,引起大量吞噬,造成细胞内胆固醇的聚集,但由MDA—LDL造成的细胞内胆固醇酯聚集可被高密度脂蛋白(HDL_3)所清除,而Ox—LDL造成的胆固醇酯聚集则不能。进一步的研究表明Ox—LDL和MDA—LDL对巨噬细胞HDL_3结合量及细胞内脂质过氧化物(LPO)含量的影响不同。虽然MDA—LDL和Ox—LDL处理巨噬细胞,都可使其HDL_3结合量有不同程度的下降,细胞内LPO含量有不同程度的升高,但当处理因素消除后,细胞继续培养时,由MDA—LDL处理的细胞其降低的HDL_3结合量又有一定的恢复,细胞LPO含量不再上升;而由Ox—LDL处理的细胞,其HDL_3结合量则继续下降,细胞LPO含量则继续升高。由Ox—LDL导致的巨噬细胞HDL_3结合量下降与细胞LPO含量升高之间呈负相关...氧化修饰低密度脂蛋白(Ox—LDL)在动脉粥样硬化发生发展中的作用越来越引起人们的重视。本文通过比较Ox—LDL和脂质过氧化降解产物丙二醛(MDA)修饰的低密度脂蛋白(MDA—LDL)在致泡沫细胞形成方面的差异,探讨了脂质过氧化对巨噬细胞的损伤在泡沫细胞形成中的作用。结果显示:Ox—LDL和MDA—LDL都可被巨噬细胞清道夫受体所识别,引起大量吞噬,造成细胞内胆固醇的聚集,但由MDA—LDL造成的细胞内胆固醇酯聚集可被高密度脂蛋白(HDL_3)所清除,而Ox—LDL造成的胆固醇酯聚集则不能。进一步的研究表明Ox—LDL和MDA—LDL对巨噬细胞HDL_3结合量及细胞内脂质过氧化物(LPO)含量的影响不同。虽然MDA—LDL和Ox—LDL处理巨噬细胞,都可使其HDL_3结合量有不同程度的下降,细胞内LPO含量有不同程度的升高,但当处理因素消除后,细胞继续培养时,由MDA—LDL处理的细胞其降低的HDL_3结合量又有一定的恢复,细胞LPO含量不再上升;而由Ox—LDL处理的细胞,其HDL_3结合量则继续下降,细胞LPO含量则继续升高。由Ox—LDL导致的巨噬细胞HDL_3结合量下降与细胞LPO含量升高之间呈负相关(r=-0.81,P<0.01)。用叔丁基脂氢过氧化物(tbooh)(1×10~(?)mol/L)对巨噬细胞损伤24小时,然后用两种修饰的LDL处理,则两种修饰LDL造成的胆固醇酯聚集都不能被HDL_3清除。本文结果提示Ox—LDL对巨噬细胞的脂质过氧化损伤可能在巨噬细胞向泡沫细胞转变过程中起着重要作用。&nbsp&&&&&相关查询
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