5TNF-alpha and IL-1 beta Neutralization Ameliorates Angiotensin II-Induced Cardiac Damage in Male Mice
文献类型：期刊论文
| 作者 | Wang, Yueli1; Li, Yulin1; Wu, Yina1; Jia, Lixin1; Wang, Jijing1; Xie, Bo2; Hui, Mizhou2; Du, Jie1 |
| 刊名 | ENDOCRINOLOGY
 |
| 出版日期 | 2014-07-01 |
| 卷号 | 155期号:7页码:2677-2687 |
| 关键词 | TUMOR-NECROSIS-FACTOR CORNEAL EPITHELIAL-CELLS TARGET ORGAN DAMAGE FACTOR-ALPHA TNF-ALPHA HEART-FAILURE ENDOTHELIAL-CELLS MONOCYTE ADHESION HYPERTENSION ROLE IL-1 PATHWAYS |
| ISSN号 | 0013-7227 |
| 其他题名 | Endocrinology |
| 中文摘要 | Inflammation is a key event in hypertensive organ damage, and TNF-alpha and IL-1 beta are elevated in hypertension. In this study, we evaluated the effects of TNF-alpha and IL-1 beta elevation on hypertensive cardiac damage by treatment with a bifunctional inflammatory inhibitor, TNF receptor 2-fragment crystalization-IL-1 receptor antagonist (TFI), which can neutralize these 2 cytokines simultaneously. A mouse hypertension model of angiotensin II (Ang II) infusion (1500 ng/kg.min for 7 d) was induced in wild-type mice. TNF-alpha and IL-1 beta were inhibited by TFI administration (5 mg/kg, every other day), the effects of inhibition on cardiac damage were examined, and its mechanism on inflammatory infiltration was further studied in vivo and in vitro. Ang II infusion induced cardiac injury, including increased macrophage infiltration, expression of inflammatory cytokines (IL-12, IL-6, etc), and cardiac fibrosis, such as elevated alpha-smooth muscle actin, collagen I, and TGF-beta expression. Importantly, the Ang II-induced cardiac injury was suppressed by TFI treatment. Moreover, TFI reduced the expression of adhesion molecules (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) and monocyte chemotactic protein-1 expression in Ang II-treated hearts. Additionally, blockade of TNF-alpha and IL-1 beta by TFI reduced monocyte adherence to endothelia cell and macrophage migration. This study demonstrates that blocking TNF-alpha and IL-1 beta by TFI prevents cardiac damage in response to Ang II, and targeting these 2 cytokines simultaneously might be a novel tool to treat hypertensive heart injury. |
| 英文摘要 | Inflammation is a key event in hypertensive organ damage, and TNF-alpha and IL-1 beta are elevated in hypertension. In this study, we evaluated the effects of TNF-alpha and IL-1 beta elevation on hypertensive cardiac damage by treatment with a bifunctional inflammatory inhibitor, TNF receptor 2-fragment crystalization-IL-1 receptor antagonist (TFI), which can neutralize these 2 cytokines simultaneously. A mouse hypertension model of angiotensin II (Ang II) infusion (1500 ng/kg.min for 7 d) was induced in wild-type mice. TNF-alpha and IL-1 beta were inhibited by TFI administration (5 mg/kg, every other day), the effects of inhibition on cardiac damage were examined, and its mechanism on inflammatory infiltration was further studied in vivo and in vitro. Ang II infusion induced cardiac injury, including increased macrophage infiltration, expression of inflammatory cytokines (IL-12, IL-6, etc), and cardiac fibrosis, such as elevated alpha-smooth muscle actin, collagen I, and TGF-beta expression. Importantly, the Ang II-induced cardiac injury was suppressed by TFI treatment. Moreover, TFI reduced the expression of adhesion molecules (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) and monocyte chemotactic protein-1 expression in Ang II-treated hearts. Additionally, blockade of TNF-alpha and IL-1 beta by TFI reduced monocyte adherence to endothelia cell and macrophage migration. This study demonstrates that blocking TNF-alpha and IL-1 beta by TFI prevents cardiac damage in response to Ang II, and targeting these 2 cytokines simultaneously might be a novel tool to treat hypertensive heart injury. |
| WOS标题词 | Science & Technology ; Life Sciences & Biomedicine |
| 类目[WOS] | Endocrinology & Metabolism |
| 研究领域[WOS] | Endocrinology & Metabolism |
| 关键词[WOS] | TUMOR-NECROSIS-FACTOR ; CORNEAL EPITHELIAL-CELLS ; TARGET ORGAN DAMAGE ; FACTOR-ALPHA ; TNF-ALPHA ; HEART-FAILURE ; ENDOTHELIAL-CELLS ; MONOCYTE ADHESION ; HYPERTENSION ROLE ; IL-1 PATHWAYS |
| 收录类别 | SCI |
| 原文出处 | |
| 语种 | 英语 |
| WOS记录号 | WOS:000342343400034 |
| 公开日期 | 2014-11-02 |
| 版本 | 出版稿 |
| 源URL | [http://ir.ipe.ac.cn/handle/122111/11659]  |
| 专题 | 过程工程研究所_研究所（批量导入） |
| 作者单位 | 1.Capital Med Univ, Beijing Anzhen Hosp, Beijing Inst Heart Lung & Blood Vessel Dis, Key Lab Remodeling Related Cardiovasc Dis,Minist, Beijing 100029, Peoples R China 2.Chinese Acad Sci, Inst Proc Engn, Natl Key Lab Biochem Engn, Beijing 100190, Peoples R China |
| 推荐引用方式 GB/T 7714 | Wang, Yueli,Li, Yulin,Wu, Yina,et al. 5TNF-alpha and IL-1 beta Neutralization Ameliorates Angiotensin II-Induced Cardiac Damage in Male Mice[J]. ENDOCRINOLOGY,2014,155(7):2677-2687. |
| APA | Wang, Yueli.,Li, Yulin.,Wu, Yina.,Jia, Lixin.,Wang, Jijing.,...&Du, Jie.(2014).5TNF-alpha and IL-1 beta Neutralization Ameliorates Angiotensin II-Induced Cardiac Damage in Male Mice.ENDOCRINOLOGY,155(7),2677-2687. |
| MLA | Wang, Yueli,et al."5TNF-alpha and IL-1 beta Neutralization Ameliorates Angiotensin II-Induced Cardiac Damage in Male Mice".ENDOCRINOLOGY 155.7(2014):2677-2687. |
入库方式： OAI收割
来源：过程工程研究所
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