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肿瘤坏死因子α和白细胞介素-10的生物学特性及其在心力衰竭中的失衡

Biology of TNFalpha and IL-10, and their imbalance in heart failure.

作者信息

Kaur Kuljeet, Dhingra Sanjiv, Slezak Jan, Sharma Anita K, Bajaj Anju, Singal Pawan K

机构信息

Department of Pharmacology, The University of Michigan, Ann Arbor, MI 48105, USA.

出版信息

Heart Fail Rev. 2009 Jun;14(2):113-23. doi: 10.1007/s10741-008-9104-z. Epub 2008 Aug 19.

DOI:10.1007/s10741-008-9104-z
PMID:18712475
Abstract

Our understanding of the multiple in vivo functions of the proinflammatory cytokine, tumor necrosis factor (TNFalpha), is advancing at a rapid pace. In addition to its antitumor effects, overproduction of TNFalpha provokes tissue injury and organ failure. TNFalpha has also been shown to be cardiodepressant and responsible for various cardiovascular complications. It appears that still much needs to be learned for a full comprehension of the role of TNFalpha in heart biology. Another cytokine, interleukin-10 (IL-10), has been shown to have anti-inflammatory properties. It is suggested to counterbalance many adverse effects of TNFalpha. IL-10 suppresses the production of TNFalpha and many other proinflammatory cytokines. TNFalpha-induced oxidative stress is also known to be mitigated by IL-10. Moreover, improvement in cardiac function after treatment with various drugs is also shown to be associated with an increase in IL-10 content. Based on the data reviewed in here, it is suggested that an optimal balance between IL-10 and TNFalpha may be a new therapeutic strategy for a healthier heart.

摘要

我们对促炎细胞因子肿瘤坏死因子(TNFα)多种体内功能的理解正在迅速推进。除了其抗肿瘤作用外,TNFα的过量产生会引发组织损伤和器官衰竭。TNFα还被证明具有心脏抑制作用,并与各种心血管并发症有关。要全面理解TNFα在心脏生物学中的作用,似乎仍有许多需要学习的地方。另一种细胞因子白细胞介素-10(IL-10)已被证明具有抗炎特性。它被认为可以抵消TNFα的许多不良反应。IL-10抑制TNFα和许多其他促炎细胞因子的产生。已知IL-10还可减轻TNFα诱导的氧化应激。此外,用各种药物治疗后心脏功能的改善也与IL-10含量的增加有关。基于所审查的数据,建议IL-10和TNFα之间的最佳平衡可能是实现心脏更健康的一种新治疗策略。

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