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|

PPARα配体对泡沫细胞炎性介质分泌的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2006年第3期
页码:
262-264,268
栏目:
基础研究
出版日期:
2006-06-25

文章信息/Info

Title:
Effect of PPARα ligands on secretion of inflammatory cytokines in foam cells
作者:
张俊峰12葛恒1郭炳诗3邵琴1王长谦1
上海交通大学附属:1.仁济医院心内科, 2.第三人民医院心内科, 上海 200000;3.上海市健康科学中心, 上海 200025
Author(s):
ZHANG Jun-feng GE Heng GUO Bing-shi SHAO Qin WANG Chang-qian
Department of Cardiology, Renji Hospital, Shanghai Jiaotong University, Shanghai 200001, China
关键词:
过氧化物酶体增殖物激活受体配体泡沫细胞炎性因子动脉粥样硬化
Keywords:
peroxisome proliferatoractivated receptorsligandsfoam cellinflammatory cytokinesatherosclerosis
分类号:
R543.5
DOI:
-
文献标识码:
A
摘要:
目的 在证实泡沫细胞有过氧化物酶体增殖物激活受体α(PPARα)表达的基础上,探讨其配体对泡沫细胞炎性介质分泌的影响。方法 体外诱导THP1单核细胞分化为巨噬细胞,给予oxLDL进一步诱导其转变为泡沫细胞,应用RTPCR检测PPARα基因表达;PPARα配体氯贝丁酯(50 μmol/L)干预后用ELISA法测定泡沫细胞培养上清液中IL6、TNF-α、MMP-2、MMP-9浓度,Gelatin Zymography测定MMPs活性。结果 巨噬细胞转化为泡沫细胞后其PPARα基因表达无显著变化;氯贝丁酯可显著抑制泡沫细胞IL-6、TNF-α(P<0.05)、MMP-9(P<0.01)的分泌,抑制MMP9的活性,对MMP-2的分泌和活性无影响。结论 PPARα配体抑制致动脉粥样硬化炎性因子的分泌,减少基质金属蛋白酶的释放并抑制其活性,对防治粥样硬化有利。
Abstract:
AIM To investigate the effect of PPARα ligands on the inflammatory cytokine secretion by foam cells. METHODS THP-1 monocytes were differentiated to macrophages in vitro and then were induced into foam cells by culturing with oxLDL. Semiquantitative RTPCR was performed to detect the expression of PPARαgene. IL-6, TNF-α, MMP-2 and MMP-9 secretion into the foam cell culture medium were measured by ELISA. MMPs activities were determined by gelatin zymography. RESULTSTreatment of oxLDL did not affect macrophage expression of PPARα. Clofibrate, a PPARα ligand, significantly inhibited the secretion of IL-6, TNF-α (P<0.05) and MMP-9 (P<0.01) by foam cells as well as MMP9 activity. MMP-2 secretion and activity were not affected. CONCLUSION PPARα ligand significantly inhibits foam cell secretion of several inflammatory molecules known to be closely associated with atherosclerotic plaque development and plaque instability. Therefore PPARα ligands may have some potential effects in the treatment of atherosclerosis.

参考文献/References

[1] Berger J, Moller DE. The mechanisms of action of PPARα[J]. Annu Rev Med, 2002, 53:409-435.

[2] Jackson SM,Parhami F, Xi XP. Peroxisome proliferatoractivated receptor activators target human endothelial cells to inhibit leukocyteendothelial cell interaction[J]. Arterioscler Thromb Vasc Biol,1999, 19(9):2094-2104.

[3] Kratky RG,Ivey J,Roach MR. Local changes in collagen content in rabbit aortic atherosclerotic lesion with time[J]. Atherosclerosis,1999,143(1):7-14.

[4] Yamada T, Sueyoshi S, Ohni S,et al. Atherosclerotic regression in the aortas of elderly. Expression of peroxisome proliferator activated receptors with references of centrally depressed atherosclerotic plaque[J]. Nippon Ronen Igakkai Zasshi, 2004,41(1):105-111.

[5] 潘晓明,吴宗贵,黄佐,等. TNFα水平对急性心肌梗死预后的影响[J]. 心脏杂志,2004,16(1):39-40.

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

[7] Ricote M, Li AC, Willson TM,et al. The peroxisome proliferator activated receptorgamma is a negative regulator of macrophage activation[J]. Nature, 1998, 391(6662):79-82.

[8] Jiang C,Ting AT,Seed B. PPARgamma agonists inhibit production of monocyte inflammatory cytokines[J]. Nature,1998,391(6662):82-86.

[9] Chinetti G, Lestavel S, Fruchart JC, et al. Peroxisome proliferatoractivated receptor alpha reduces cholesterol esterification in macrophages[J]. Circ Res,2003, 92(2):212-217.

备注/Memo

备注/Memo:
收稿日期:2005-07-12.基金项目:国家自然科学基金项目资助(No.30070869) 通讯作者:王长谦,教授,主要从事动脉粥样硬化防治研究 Email:changqianwang@hotmail.com. 作者简介:张俊峰,主治医师,硕士 Tel:(021)566911016260 Email:zhangjf1222@yahoo.com.cn.
更新日期/Last Update: