我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

孤儿核受体Nur77对氧化型低密度脂蛋白诱导的 小鼠巨噬细胞系分泌炎症因子的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2008年第5期
页码:
541-544
栏目:
基础研究
出版日期:
2008-10-20

文章信息/Info

Title:
Effect of orphan nuclear receptor Nur77 on inflammatory factor secretion in murine macrophage strain
作者:
胡刘华1; 何奔1; 沈玲红1; 江立生1; 柴大军1; 王力2; 曾锦章2
1.上海交通大学医学院附属仁济医院心内科，上海 200127； 2.中科院上海生命科学研究院生茂联合研发中心,上海 200233
Author(s):
HU Liuhua1;  HE Ben1;  SHEN Linghong1;  JIANG Lisheng1;  CHAI Dajun1;  WANG Li2;  ZENG Jinzhang2
1.Department of Cardiology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China; 2.SAMOST GROUP Union R & D Center, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200233, China
关键词:
孤儿核受体; 氧化型低密度脂蛋白; 巨噬细胞; 炎症因子; 小鼠
Keywords:
orphan nuclear receptor;  oxLDL;  macrophage;  inflammatory factor;  mouse
分类号:
R513.5
DOI:
-
文献标识码:
A
摘要:
目的 观察孤儿核受体Nur77对氧化型低密度脂蛋白（ox-LDL）诱导小鼠巨噬细胞分泌炎症因子的影响。方法 建立稳定转染GFPNur77质粒的小鼠巨噬细胞系RAW264.7，并以稳定转染绿色荧光蛋白（GFP）基因的细胞系RAW264.7作为对照。将转染的细胞与ox-LDL（40 mg/L）共同孵育24 h后，采用ELISA法检测炎症因子TNF-α、IFN-γ、基质金属蛋白酶-9（MMP-9）、单核细胞趋化蛋白-1（MCP-1）和IL-6的表达。 结果 经ox-LDL刺激后，不同质粒DNA转染的两种细胞中，IFN-γ、TNF-α、MMP-9和MCP-1的浓度均升高（P<0.05）；但GFP-Nur77-RAW264.7细胞的增长水平明显低于GFPRAW2647细胞（P<0.05）。oxLDL刺激前，GFP-RAW264.7细胞分泌的4种炎症因子（TNF-α、IFN-γ、MMP-9和MCP-1）的浓度，分别为（19.00±1.69）ng/L、（99.10±309）ng/L、（0.14±0.02）ng/L和（23.96±3.57）ng/L；oxLDL刺激后，分别上升为（27.22±0.38）ng/L、（549.90±1.81）ng/L、（0.45±0.06）ng/L和（49.31±3.66）ng/L。ox-LDL刺激前，GFP-Nur77-RAW264.7和GFP-RAW264.7细胞分泌的4种炎症因子的浓度无统计学的差异性。ox-LDL刺激后，4种炎症因子的浓度分别上升为（18.34±1.06）ng/L、（320.56±1.27）ng/L、（0.20±0.03）ng/L和（38.92±4.46）ng/L。而两种细胞（CTFP-Nur77-RAW264.7细胞与GFP-RAW264.7细胞）分泌IL-6的浓度未见显著差异。 结论 RAW264.7细胞中Nur77表达的上调,能够显著减少ox-LDL诱导的炎症因子（IL-6除外）分泌，这可能是孤儿核受体Nur77心血管保护作用的重要机制之一。
Abstract:
AIM To observe the effect of orphan nuclear receptor Nur77 on inflammatory factor secretion in murine macrophage RAW264.7 induced by oxidized low density lipoprotein (ox-LDL). METHODS RAW264.7 cells stably expressing transfecting plasmid GFPNur77 and GFP cDNA (as a control) were respectively established. After the two transfected macrophages were incubated with ox-LDL (40 mg/L), the concentrations of TNF-α, IFN-γ, MMP-9, MCP-1 and IL-6 in culture supernatant were detected by ELISA. RESULTSAfter the oxLDL stimulation, the concentrations of IFN-γ, TNF-α, MMP-9 and MCP-1 in the two transfected macrophages all increased (P<005). However, the increased concentrations in GFP-Nur77-RAW264.7 were significantly less than those in GFPRAW264.7 (P<0.05). Before ox-LDL stimulation, the concentrations of TNF-α, IFN-γ, MMP-9 and Mcp-1 in GFP-RAW264.7 were respectively (19.00±1.69)ng/L, (99.10±3.09)ng/L, (0.14±0.02)ng/L and (23.96±3.57)ng/L After the stimulation, the concentrations of the 4 inflammatury factors increased to (27.22±0.38)ng/L, (549.90±1.81)ng/L, (0.45±0.06)ng/L and (49.31±3.66)ng/L respectively. Before ox-LDL stimulation, the concentrations of the 4 inflammatory factors secreted by GFP-Nur77-RAW264.7 and GFPRAW264.7 had no statistical difference. After oxLDL stimuladtion, the concentrations of the 4 inflammatory factors increased to (18.34±1.06)ng/L, (320.56±127)ng/L, (0.20±0.03)ng/L and (38.92±4.46)ng/L respectively. However, no significant changes were observed in IL6 concentration secreted by GFP-Nur77-RAW264.7 or GFP-RAW264.7. CONCLUSION High expression of Nur77 on RAW264.7 cells obviously reduce the inflammatory factor secretion induced by ox-LDL. This may be an important protective mechanism of Nur77.

参考文献/References

［1］ Libby P, Ridker PM, Maseft A. Inflammation and atherosclerosis［J］. Circulation, 2002, 105(9):1135-1143.

［2］ Rius J, MartinezGonzalez J, Crespo J, et al. Involvement of neuronderived orphan receptor1 (NOR1) in LDLinduced mitogenic stimulus in vascular smooth muscle cells: role of CREB［J］. Arterioscler Thromb Vasc Biol, 2004, 24(4):697-702.

［3］ Bonta PI, van Tiel CM, Vos M, et al. Nuclear receptors Nur77, Nurr1, and NOR1 expressed in atherosclerotic lesion macrophages reduce lipid loading and inflammatory responses［J］. Arterioscler Thromb Vasc Biol, 2006, 26(10):2288-2294.

［4］ Han CY, Par YK. Oxidationdependent effects of oxidized LDL: proliferation or cell death［J］. Exp Mol Med, 1999, 31(4): 165-173.

［5］ PiSunyer FX. The relation of adipose tissue to cardiometabolic risk［J］. Clin Cornerstone, 2006, 8 Suppl 4:S14-S23.

［6］ Szabo SJ, Sullivan BM, Peng SL, et al. Molecular mechanisms regulating Th1 immune responses［J］. Annu Rev Immunol, 2003, 21:713-758.

［7］ Hamnon JR. The role of MCP1 in atherosclerosis［J］. Stem Cells, 2000, 18(1)：65-66.

［8］ Hsueh WA, Jackson S, Ronald E. Control of vascrlar cell proliferation and migration by PPAR ［J］ . Diabetes Care, 2001, 24(2): 392-397.

［9］ Cheng LE, Chan FK, Cado D, et al. Functional redundancy of the Nur77 and Nor1 orphan steroid receptors in Tcell apoptosis ［J］. EMBO J, 1997, 16(8):1865-1875.

［10］Li H, Kolluri SK, Gu J, et al. Cytochrome c release and apoptosis induced by mitochondrial targeting of nuclear orphan receptor TR3 ［J］. Science, 2000, 289(5482):1159-1164.

［11］Lin B, Kolluri SK, Lin F, et al. Conversion of Bcl2 from protector to killer by interaction with nuclear orphan receptor Nur77/TR3［J］. Cell, 2004, 116(4):527-540.

［12］Pei L, Castrillo A, Chen M, et al. Induction of NR4A orphan nuclear receptor expression in macrophages in response to inflammatory stimuli ［J］. J Biol Chem, 2005, 280(32):29256-29262.

备注/Memo

备注/Memo:
收稿日期：2008-01-30.基金项目：国家自然科学基金项目资助（30670880） 通讯作者：何奔，教授，主任医师，主要从事冠心病介入治疗和核受体在动脉粥样硬化中的作用机制研究 Email:heben@medmail.com.cn 作者简介：胡刘华，硕士生Email:iam565@126.com
更新日期/Last Update: