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学科主题: 临床医学
题名:
Inhibition of Tumor Necrosis Factor-alpha-Induced Interleukin-6 Expression by Telmisartan Through Cross-Talk of Peroxisome Proliferator-Activated Receptor-gamma With Nuclear Factor kappa B and CCAAT/Enhancer- Binding Protein-beta
作者: Tian, Qingping3; Miyazaki, Ryohei; Ichiki, Toshihiro1,2; Imayama, Ikuyo; Inanaga, Keita; Ohtsubo, Hideki; Yano, Kotaro; Takeda, Kotaro2; Sunagawa, Kenji
关键词: interleukin-6 ; TNF-alpha ; PPAR gamma ; NF-kappa B ; C/EBP beta
刊名: HYPERTENSION
发表日期: 2009-05-01
DOI: 10.1161/HYPERTENSIONAHA.108.126656
卷: 53, 期:5, 页:798-804
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Peripheral Vascular Disease
研究领域[WOS]: Cardiovascular System & Cardiology
关键词[WOS]: SMOOTH-MUSCLE-CELLS ; CONVERTING-ENZYME-INHIBITORS ; C-REACTIVE PROTEIN ; ANGIOTENSIN-II ; PPAR-GAMMA ; HEART-FAILURE ; C/EBP-BETA ; BLOCKERS ; DISEASE ; GENE
英文摘要:

Telmisartan, an angiotensin II type 1 receptor antagonist, was reported to be a partial agonist of peroxisome proliferator-activated receptor-gamma. Although peroxisome proliferator-activated receptor-gamma activators have been shown to have an anti-inflammatory effect, such as inhibition of cytokine production, it has not been determined whether telmisartan has such effects. We examined whether telmisartan inhibits expression of interleukin-6 (IL-6), a proinflammatory cytokine, in vascular smooth muscle cells. Telmisartan, but not valsartan, attenuated IL-6 mRNA expression induced by tumor necrosis factor-alpha (TNF-alpha). Telmisartan decreased TNF-alpha-induced IL-6 mRNA and protein expression in a dose-dependent manner. Because suppression of IL-6 mRNA expression was prevented by pretreatment with GW9662, a specific peroxisome proliferator-activated receptor-gamma antagonist, peroxisome proliferator-activated receptor-gamma may be involved in the process. Telmisartan suppressed IL-6 gene promoter activity induced by TNF-alpha. Deletion analysis suggested that the DNA segment between -150 bp and -27 bp of the IL-6 gene promoter that contains nuclear factor kappa B and CCAAT/enhancer-binding protein-beta sites was responsible for telmisartan suppression. Telmisartan attenuated TNF-alpha-induced nuclear factor kappa B- and CCAAT/enhancer-binding protein-beta-dependent gene transcription and DNA binding. Telmisartan also attenuated serum IL-6 level in TNF-alpha-infused mice and IL-6 production from rat aorta stimulated with TNF-alpha ex vivo. These data suggest that telmisartan may attenuate inflammatory process induced by TNF-alpha in addition to the blockade of angiotensin II type 1 receptor. Because both TNF-alpha and angiotensin II play important roles in atherogenesis through enhancement of vascular inflammation, telmisartan may be beneficial for treatment of not only hypertension but also vascular inflammatory change. (Hypertension. 2009; 53: 798-804.)

语种: 英语
所属项目编号: 19590867
项目资助者: Ministry of Education, Culture, Sports, Science and Technology of Japan ; Japan-China Sasakawa Medical Fellowship
WOS记录号: WOS:000265450400011
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/57169
Appears in Collections:北京大学第一临床医学院_期刊论文

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作者单位: 1.Kyushu Univ, Grad Sch Med Sci, Dept Cardiovasc Med, Higashi Ku, Fukuoka 8128582, Japan
2.Kyushu Univ, Grad Sch Med Sci, Dept Adv Therapeut Cardiovasc Dis, Fukuoka 8128582, Japan
3.Peking Univ, Hosp 1, Fukuoka, Japan

Recommended Citation:
Tian, Qingping,Miyazaki, Ryohei,Ichiki, Toshihiro,et al. Inhibition of Tumor Necrosis Factor-alpha-Induced Interleukin-6 Expression by Telmisartan Through Cross-Talk of Peroxisome Proliferator-Activated Receptor-gamma With Nuclear Factor kappa B and CCAAT/Enhancer- Binding Protein-beta[J]. HYPERTENSION,2009,53(5):798-804.
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